subject:(innate immunity)

University of Georgia

1. Connor, Meghan Ashley. Role of a novel pattern recognition receptor in antibacterial innate immunity.

Degree: MS, Infectious Diseases, 2008, University of Georgia

URL: http://purl.galileo.usg.edu/uga_etd/connor_meghan_a_200805_ms

► Teleosts are an evolutionarily appropriate model for studying immunology. The innate immune system of fish is the principal defense mechanism. The acquired immune system is… (more)

Subjects/Keywords: Innate Immunity

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APA (6^th Edition):

Connor, M. A. (2008). Role of a novel pattern recognition receptor in antibacterial innate immunity. (Masters Thesis). University of Georgia. Retrieved from http://purl.galileo.usg.edu/uga_etd/connor_meghan_a_200805_ms

Chicago Manual of Style (16^th Edition):

Connor, Meghan Ashley. “Role of a novel pattern recognition receptor in antibacterial innate immunity.” 2008. Masters Thesis, University of Georgia. Accessed January 19, 2020. http://purl.galileo.usg.edu/uga_etd/connor_meghan_a_200805_ms.

MLA Handbook (7^th Edition):

Connor, Meghan Ashley. “Role of a novel pattern recognition receptor in antibacterial innate immunity.” 2008. Web. 19 Jan 2020.

Vancouver:

Connor MA. Role of a novel pattern recognition receptor in antibacterial innate immunity. [Internet] [Masters thesis]. University of Georgia; 2008. [cited 2020 Jan 19]. Available from: http://purl.galileo.usg.edu/uga_etd/connor_meghan_a_200805_ms.

Council of Science Editors:

Connor MA. Role of a novel pattern recognition receptor in antibacterial innate immunity. [Masters Thesis]. University of Georgia; 2008. Available from: http://purl.galileo.usg.edu/uga_etd/connor_meghan_a_200805_ms

University of Alberta

2. Guntermann, Silvia. Caspase activity and regulation in Drosophila melanogaster innate immunity.

Degree: PhD, Department of Medical Microbiology and Immunology, 2014, University of Alberta

URL: https://era.library.ualberta.ca/files/cr207tp490

► The fine balance struck between life and death is key for the health of all multicellular organisms and therefore the pathways that govern life and… (more)

▼ The fine balance struck between life and death is key for the health of all multicellular organisms and therefore the pathways that govern life and death decisions are evolutionarily highly conserved. For example, the human TNF and the Drosophila IMD pathways coordinate signaling elements such as conserved JNK, NF-κB, and caspase modules to drive appropriate responses. Caspases are an evolutionarily conserved family of cysteinyl aspartate proteases with fundamental roles in the opposing processes of cell-survival and cell-death. The caspase Dredd is an essential pro-survival regulator of the IMD mediated immune response. However, the detailed involvement of Dredd in the sequential activation of the IMD cascade, the position of Dredd, and Dredd’s interactions with the IMD pathway were unknown. In addition, the molecular mechanism of Dredd activation and regulation was unclear. In this study I conducted a thorough structural and functional analysis of the mechanism of Dredd activity in IMD signaling. I revealed numerous interactions of Dredd with early activators of the IMD pathway. I showed that the caspase activity inhibitor p35 blocked Dredd activation in a mechanism that is distinct from the general mechanism of p35- dependent caspase inhibition. In addition, Dredd activation appears independent of auto-processing which might be explained by the lack of Dredd linker residues that support auto-processing and may explain Dredd’s sole function in pro- survival responses. In a combination of cell culture and in vivo assays, I demonstrated that Dredd is required for the activation of dJNK signaling upstream of dTAK1 and determined that Dredd additionally functions down- stream of Imd activation. Furthermore, my data uncovered a dual regulation of dIAP2 by RING domain mediated destruction and Dronc mediated N-terminal proteolytic cleavage. In summary, the data indicate a distinct activation mechanism for Dredd and establish dual functions for Dredd in the IMD signaling cascade, where Dredd is required in a proximal signaling complex for the early transduction of a phospho-relay to Rel and dJNK as well as for the subsequent activation of Rel. The data also uncover a novel role for Dronc in immune signaling. Combined the findings underline the importance and complexity of non-apoptotic roles of caspases.

Subjects/Keywords: innate immunity; caspase

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APA (6^th Edition):

Guntermann, S. (2014). Caspase activity and regulation in Drosophila melanogaster innate immunity. (Doctoral Dissertation). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/cr207tp490

Chicago Manual of Style (16^th Edition):

Guntermann, Silvia. “Caspase activity and regulation in Drosophila melanogaster innate immunity.” 2014. Doctoral Dissertation, University of Alberta. Accessed January 19, 2020. https://era.library.ualberta.ca/files/cr207tp490.

MLA Handbook (7^th Edition):

Guntermann, Silvia. “Caspase activity and regulation in Drosophila melanogaster innate immunity.” 2014. Web. 19 Jan 2020.

Vancouver:

Guntermann S. Caspase activity and regulation in Drosophila melanogaster innate immunity. [Internet] [Doctoral dissertation]. University of Alberta; 2014. [cited 2020 Jan 19]. Available from: https://era.library.ualberta.ca/files/cr207tp490.

Council of Science Editors:

Guntermann S. Caspase activity and regulation in Drosophila melanogaster innate immunity. [Doctoral Dissertation]. University of Alberta; 2014. Available from: https://era.library.ualberta.ca/files/cr207tp490

University of Manitoba

3. Rahman, Rahmat Naureen. JNK- associated leucine zipper (JLP) scaffolding protein regulates natural killer cell migrations.

Degree: Immunology, 2019, University of Manitoba

URL: http://hdl.handle.net/1993/33778

► JNK-associated leucine zipper protein (JLP) is a scaffold protein in the Mitogen-activated protein kinase (MAPK) known to be essential for mediating MAPK functions= such as… (more)

Subjects/Keywords: Immunology; Innate Immunity

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APA (6^th Edition):

Rahman, R. N. (2019). JNK- associated leucine zipper (JLP) scaffolding protein regulates natural killer cell migrations. (Masters Thesis). University of Manitoba. Retrieved from http://hdl.handle.net/1993/33778

Chicago Manual of Style (16^th Edition):

Rahman, Rahmat Naureen. “JNK- associated leucine zipper (JLP) scaffolding protein regulates natural killer cell migrations.” 2019. Masters Thesis, University of Manitoba. Accessed January 19, 2020. http://hdl.handle.net/1993/33778.

MLA Handbook (7^th Edition):

Rahman, Rahmat Naureen. “JNK- associated leucine zipper (JLP) scaffolding protein regulates natural killer cell migrations.” 2019. Web. 19 Jan 2020.

Vancouver:

Rahman RN. JNK- associated leucine zipper (JLP) scaffolding protein regulates natural killer cell migrations. [Internet] [Masters thesis]. University of Manitoba; 2019. [cited 2020 Jan 19]. Available from: http://hdl.handle.net/1993/33778.

Council of Science Editors:

Rahman RN. JNK- associated leucine zipper (JLP) scaffolding protein regulates natural killer cell migrations. [Masters Thesis]. University of Manitoba; 2019. Available from: http://hdl.handle.net/1993/33778

Texas A&M University

4. Jiang, Shan. Plant Defense Signaling Mechanisms and Evolution.

Degree: 2015, Texas A&M University

URL: http://hdl.handle.net/1969.1/155604

► Plant innate immunity has been classified into two layers of defense systems. Nucleotide-binding domain leucine-rich repeat (NLR) protein complexes activated by pathogen effectors launches effector-triggered… (more)

▼ Plant innate immunity has been classified into two layers of defense systems. Nucleotide-binding domain leucine-rich repeat (NLR) protein complexes activated by pathogen effectors launches effector-triggered immunity (ETI). A forward genetic screen using the ETI marker gene WRKY46 promoter fused with a firefly luciferase gene (pWRKY46::LUC) as a reporter identified five ARABIDOPSIS GENES GOVERNING IMMUNE GENE EXPRESSION (aggie) mutants, named as aggie4-8. Though with elevated pWRKY46::LUC activity, aggie4 showed enhanced resistance to avirulent bacterial infections, yet delayed hypersensitive response (HR), while aggie5 exhibited compromised disease resistance and delayed HR. Map-based cloning coupled with next generation sequencing (NGS) suggests that causal mutations of aggie4 and aggie5 locate in different regions of chromosome 5. In addition, pWRKY46::LUC activity is elevated in aggie6 and aggie7, while suppressed in aggie8. Perception of microbe-associated molecular patterns (MAMPs) by pattern recognition receptors (PRRs) triggers another tier of innate immunity, termed as pattern-triggered immunity (PTI). The Arabidopsis SOMATIC EMBRYOGENESIS RECEPTOR KINASE (SERK) family plays important roles in plant defense responses. It remains unknown how SERK members have evolved. Here, three SERK homologs, Pp1s35_219V6.1, Pp1s96_90V6.1 and Pp1s118_79V6.1 were identified in P. Patens with 60%-80% amino acid identify to AtSERKs and were named as PpSERK1.1, PpSERK1.2 and PpSERK2 respectively. In vitro kinase assay revealed that PpSERK1.1 and PpSERK1.2, but not PpSERK2, possess strong kinase activity. Functional complementation analysis suggested that PpSERK1.1 and PpSERK1.2 but not PpSERK2 regulate FLS2-mediated plant defense, and PpSERK1.2 but not PpSERK1.1 also regulates cell death in Arabidopsis. PTI induces a rapid and profound transcriptional reprograming via concerted actions of specific transcription factors and general transcription machinery. Arabidopsis SH4-related 3 (ASR3), a plant specific trihelix family of transcription factors, is rapidly phosphorylated by MPK4 at Threonine 189 residue upon multiple MAMP treatments but not upon elicitation of ETI. Genetic and biochemical data suggests that phosphorylation of ASR3 enhances its DNA binding activity to suppress immune genes expression. Importantly, the asr3 mutant shows higher immune gene activation and enhanced disease resistance, while transgenic plants overexpressing ASR3 exhibit compromised PTI responses. This study reveals that ASR3 functions as a transcription repressor regulated by MPK4 to fine-tune plant defense. Advisors/Committee Members: Shan, Libo (advisor), He, Ping (committee member), Kenerley, Charles (committee member), Figueiredo, Paul de (committee member).

Subjects/Keywords: Plant defense; innate immunity; evolution

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APA (6^th Edition):

Jiang, S. (2015). Plant Defense Signaling Mechanisms and Evolution. (Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/155604

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Jiang, Shan. “Plant Defense Signaling Mechanisms and Evolution.” 2015. Thesis, Texas A&M University. Accessed January 19, 2020. http://hdl.handle.net/1969.1/155604.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Jiang, Shan. “Plant Defense Signaling Mechanisms and Evolution.” 2015. Web. 19 Jan 2020.

Vancouver:

Jiang S. Plant Defense Signaling Mechanisms and Evolution. [Internet] [Thesis]. Texas A&M University; 2015. [cited 2020 Jan 19]. Available from: http://hdl.handle.net/1969.1/155604.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Jiang S. Plant Defense Signaling Mechanisms and Evolution. [Thesis]. Texas A&M University; 2015. Available from: http://hdl.handle.net/1969.1/155604

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

5. Ramyar, Kasra Xerxes. Biochemical Characterization of Murine Qa-1.

Degree: 2014, Johns Hopkins University

URL: http://jhir.library.jhu.edu/handle/1774.2/37158

► Qa-1 is a member of the mouse MHC Ib family with roles in both the adaptive and innate arms of immunity. While it is presumed… (more)

Subjects/Keywords: Innate Immunity Immune Surveillance

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APA (6^th Edition):

Ramyar, K. X. (2014). Biochemical Characterization of Murine Qa-1. (Thesis). Johns Hopkins University. Retrieved from http://jhir.library.jhu.edu/handle/1774.2/37158

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Ramyar, Kasra Xerxes. “Biochemical Characterization of Murine Qa-1.” 2014. Thesis, Johns Hopkins University. Accessed January 19, 2020. http://jhir.library.jhu.edu/handle/1774.2/37158.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Ramyar, Kasra Xerxes. “Biochemical Characterization of Murine Qa-1.” 2014. Web. 19 Jan 2020.

Vancouver:

Ramyar KX. Biochemical Characterization of Murine Qa-1. [Internet] [Thesis]. Johns Hopkins University; 2014. [cited 2020 Jan 19]. Available from: http://jhir.library.jhu.edu/handle/1774.2/37158.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Ramyar KX. Biochemical Characterization of Murine Qa-1. [Thesis]. Johns Hopkins University; 2014. Available from: http://jhir.library.jhu.edu/handle/1774.2/37158

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Hawaii – Manoa

6. Yang, Baojun. Cellular response of insect cells to virus infection.

Degree: 2015, University of Hawaii – Manoa

URL: http://hdl.handle.net/10125/100551

►

Ph.D. University of Hawaii at Manoa 2014.

RNA interference (RNAi) is the dsRNA-triggered gene regulatory mechanism that is evolutionally conserved in most eukaryotic cells. It… (more)

▼

Ph.D. University of Hawaii at Manoa 2014.

RNA interference (RNAi) is the dsRNA-triggered gene regulatory mechanism that is evolutionally conserved in most eukaryotic cells. It has been widely used as a powerful tool for functional genomics in various organisms. In flies, mosquitoes or other insect cells, gene functional analysis by RNAi is usually performed through introduced dsRNAs that are synthesized by in vitro transcription. RNAi serves as an important innate immunity against viruses in plants and invertebrates. It has recently been shown that Aedes albopictus mosquito C6/36 cells, commonly used for arbovirus propagation, possess an impaired RNAi pathway. In this study, we developed in vitro Dicer assay using extracts prepared from mosquito cells. Our results confirmed the inability of C6/36 cells to process dsRNAs into siRNAs, which is consistent with the loss-of-function of Dcr-2 due to a frameshift mutation. However, such a defect could not be complemented by introduction of Drosophila Dicer-2. To evaluate the RNAi-based antiviral mechanism in C6/36 cells, we analyzed the replication of a mutant Nodamura virus (NoV) genomic RNA1 of which viral RNAi suppressor B2 is not expressed (NoVR1ΔB2) and cannot accumulate to a detectable level in RNAi-competent cells. In C6/36 cells, the defective RNAi gives rise to complete restoration of NoVR1ΔB2 replication, suggesting that RNAi is the primary antiviral immunity in mosquito cells. At present, dsRNA, as the trigger of the antiviral RNAi pathway in invertebrate and plants, is the major efficiency limitation factor in RNAi. In this study, a plasmid-based system was developed to express dsRNA intracellular from a DNA cassette containing two convergent T7 promoters in Drosophila S2 cells. Efficient knockdown of a transiently expressed reporter gene or an endogenous gene can be achieved by dsRNA expressed from the system. A random cDNA library was constructed in the dsRNA expression cassette and initial screening led to identification of two host factors that are involved in antiviral response in Drosophila S2 cells. The plasmid-based dsRNA expression system provides an alternative tool for functional genomics in Drosophila and other insect cells.

Subjects/Keywords: Antiviral; dsRNA; RNAi; Innate Immunity

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APA (6^th Edition):

Yang, B. (2015). Cellular response of insect cells to virus infection. (Thesis). University of Hawaii – Manoa. Retrieved from http://hdl.handle.net/10125/100551

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Yang, Baojun. “Cellular response of insect cells to virus infection.” 2015. Thesis, University of Hawaii – Manoa. Accessed January 19, 2020. http://hdl.handle.net/10125/100551.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Yang, Baojun. “Cellular response of insect cells to virus infection.” 2015. Web. 19 Jan 2020.

Vancouver:

Yang B. Cellular response of insect cells to virus infection. [Internet] [Thesis]. University of Hawaii – Manoa; 2015. [cited 2020 Jan 19]. Available from: http://hdl.handle.net/10125/100551.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Yang B. Cellular response of insect cells to virus infection. [Thesis]. University of Hawaii – Manoa; 2015. Available from: http://hdl.handle.net/10125/100551

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Rochester

7. Aggrey, Angela Akosua. A Novel Protective Role for Platelet-Mediated Immune Responses in Murine Experimental Cerebral Malaria.

Degree: PhD, 2013, University of Rochester

URL: http://hdl.handle.net/1802/27239

► Cerebral malaria is caused by complications from Plasmodium falciparum infection and claims hundreds of thousands of lives of young children in endemic countries annually. Platelets… (more)

Subjects/Keywords: Platelets; Innate Immunity, Malaria; Inflammation

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APA (6^th Edition):

Aggrey, A. A. (2013). A Novel Protective Role for Platelet-Mediated Immune Responses in Murine Experimental Cerebral Malaria. (Doctoral Dissertation). University of Rochester. Retrieved from http://hdl.handle.net/1802/27239

Chicago Manual of Style (16^th Edition):

Aggrey, Angela Akosua. “A Novel Protective Role for Platelet-Mediated Immune Responses in Murine Experimental Cerebral Malaria.” 2013. Doctoral Dissertation, University of Rochester. Accessed January 19, 2020. http://hdl.handle.net/1802/27239.

MLA Handbook (7^th Edition):

Aggrey, Angela Akosua. “A Novel Protective Role for Platelet-Mediated Immune Responses in Murine Experimental Cerebral Malaria.” 2013. Web. 19 Jan 2020.

Vancouver:

Aggrey AA. A Novel Protective Role for Platelet-Mediated Immune Responses in Murine Experimental Cerebral Malaria. [Internet] [Doctoral dissertation]. University of Rochester; 2013. [cited 2020 Jan 19]. Available from: http://hdl.handle.net/1802/27239.

Council of Science Editors:

Aggrey AA. A Novel Protective Role for Platelet-Mediated Immune Responses in Murine Experimental Cerebral Malaria. [Doctoral Dissertation]. University of Rochester; 2013. Available from: http://hdl.handle.net/1802/27239

Universiteit Utrecht

8. Hogenkamp, A. Collectins in innate immune defense of pigs and chickens.

Degree: 2007, Universiteit Utrecht

URL: http://dspace.library.uu.nl:8080/handle/1874/23210

► In the Netherlands, the number of chickens and pigs exceeds the number of human inhabitants by far. Therefore, combating infections in livestock is not only… (more)

▼ In the Netherlands, the number of chickens and pigs exceeds the number of human inhabitants by far. Therefore, combating infections in livestock is not only of economical importance, but also of great importance to public health. The innate immune system provides a first line defense against infectious pathogens, and its effector mechanisms rely on the recognition of features that are common to many pathogens. These features, known as pathogen-associated molecular patterns can be recognized by pattern recognition molecules at the site of infection, which is often an epithelial surface like the lung, skin or gastro-intestinal tract. Collectins, an important group of pattern recognition molecules, have been reported to be expressed in many epithelial surfaces. In the lung, Surfactant Protein-D (SP-D) contributes to the maintenance of a sterile respiratory system. Its role in the gastro-intestinal tract, which is dominated by the presence of micro-organisms, is less clear. Therefore, we investigated the interaction of porcine SP-D (pSP-D) with various Gram-negative bacteria isolated from the porcine intestine. It was shown that while pSP-D is capable of reducing growth rates of E. coli K12, the growth rates and survival of pathogenic bacterial strains isolated from the porcine intestine remained unaffected. Furthermore, pSP-D was shown to affect bacterial adhesion- and invasion- characteristics, leading to a significant increase in adhesion and invasion of bacteria into IPI-I2 cells. It is not yet clear what the mechanism behind these effects is, but it could reflect a scavenger function for pSP-D in the intestine. In the chicken, only two collectins had been described thus far. In this thesis, we report the discovery of three new chicken collectins, chicken Collectin 1-3 (cCL-1, -2,and -3) and one chicken lectin, chicken Lung Lectin (cLL). Results from this study support the assumption that cCL-1, -2 and -3, together with their respective mammalian homologues CL-L1, CL-K1 and CL-P1 represent three new unique classes within the collectin protein family. Because of its predominant expression in the chicken respiratory tract, the newly discovered chicken lectin was designated chicken Lung Lectin (cLL). To investigate whether these chicken (col)lectins are involved in avian innate immunity, their mRNA expression levels during bacterial and viral infections were investigated. Samples derived from three infection-models were analyzed, and the results showed that mRNA expression of chicken (col)lectins cCL-1, cCL-2, cSP-A and cLL can be affected by both bacterial and viral infections. We also investigated the structural and functional aspects of cLL. To this end, recombinant cLL was successfully produced in HEK-293 EBNA cells. Characterization of recombinant cLL revealed that this protein is capable of binding sugars, and, as predicted from its sequence, does so in a calcium-dependent manner. In addition, cLL showed anti-viral activity against avian IAV in our preliminary tests, and HAA-inhibition of a human isolate of IAV…

Subjects/Keywords: Diergeneeskunde; collectin; innate immunity; chicken

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APA (6^th Edition):

Hogenkamp, A. (2007). Collectins in innate immune defense of pigs and chickens. (Doctoral Dissertation). Universiteit Utrecht. Retrieved from http://dspace.library.uu.nl:8080/handle/1874/23210

Chicago Manual of Style (16^th Edition):

Hogenkamp, A. “Collectins in innate immune defense of pigs and chickens.” 2007. Doctoral Dissertation, Universiteit Utrecht. Accessed January 19, 2020. http://dspace.library.uu.nl:8080/handle/1874/23210.

MLA Handbook (7^th Edition):

Hogenkamp, A. “Collectins in innate immune defense of pigs and chickens.” 2007. Web. 19 Jan 2020.

Vancouver:

Hogenkamp A. Collectins in innate immune defense of pigs and chickens. [Internet] [Doctoral dissertation]. Universiteit Utrecht; 2007. [cited 2020 Jan 19]. Available from: http://dspace.library.uu.nl:8080/handle/1874/23210.

Council of Science Editors:

Hogenkamp A. Collectins in innate immune defense of pigs and chickens. [Doctoral Dissertation]. Universiteit Utrecht; 2007. Available from: http://dspace.library.uu.nl:8080/handle/1874/23210

9. 舟見, 健児. Toll-like receptor 3の細胞内局在、及びシグナル伝達に関与する機能ドメインの同定 : The cytoplasmic "linker region" in Toll-like receptor 3 controls receptor licalization and signaling; Toll-like receptor 3 ノサイボウナイキョクザイオヨビシグナルデンタツニカンヨスルキノウドメインノドウテイ.

Degree: Nara Institute of Science and Technology / 奈良先端科学技術大学院大学

URL: http://hdl.handle.net/10061/2831

Subjects/Keywords: Innate immunity

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APA (6^th Edition):

舟見, �. (n.d.). Toll-like receptor 3の細胞内局在、及びシグナル伝達に関与する機能ドメインの同定 : The cytoplasmic "linker region" in Toll-like receptor 3 controls receptor licalization and signaling; Toll-like receptor 3 ノサイボウナイキョクザイオヨビシグナルデンタツニカンヨスルキノウドメインノドウテイ. (Thesis). Nara Institute of Science and Technology / 奈良先端科学技術大学院大学. Retrieved from http://hdl.handle.net/10061/2831

Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

舟見, 健児. “Toll-like receptor 3の細胞内局在、及びシグナル伝達に関与する機能ドメインの同定 : The cytoplasmic "linker region" in Toll-like receptor 3 controls receptor licalization and signaling; Toll-like receptor 3 ノサイボウナイキョクザイオヨビシグナルデンタツニカンヨスルキノウドメインノドウテイ.” Thesis, Nara Institute of Science and Technology / 奈良先端科学技術大学院大学. Accessed January 19, 2020. http://hdl.handle.net/10061/2831.

Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

舟見, 健児. “Toll-like receptor 3の細胞内局在、及びシグナル伝達に関与する機能ドメインの同定 : The cytoplasmic "linker region" in Toll-like receptor 3 controls receptor licalization and signaling; Toll-like receptor 3 ノサイボウナイキョクザイオヨビシグナルデンタツニカンヨスルキノウドメインノドウテイ.” Web. 19 Jan 2020.

Note: this citation may be lacking information needed for this citation format:
No year of publication.

Vancouver:

舟見 �. Toll-like receptor 3の細胞内局在、及びシグナル伝達に関与する機能ドメインの同定 : The cytoplasmic "linker region" in Toll-like receptor 3 controls receptor licalization and signaling; Toll-like receptor 3 ノサイボウナイキョクザイオヨビシグナルデンタツニカンヨスルキノウドメインノドウテイ. [Internet] [Thesis]. Nara Institute of Science and Technology / 奈良先端科学技術大学院大学; [cited 2020 Jan 19]. Available from: http://hdl.handle.net/10061/2831.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.

Council of Science Editors:

舟見 �. Toll-like receptor 3の細胞内局在、及びシグナル伝達に関与する機能ドメインの同定 : The cytoplasmic "linker region" in Toll-like receptor 3 controls receptor licalization and signaling; Toll-like receptor 3 ノサイボウナイキョクザイオヨビシグナルデンタツニカンヨスルキノウドメインノドウテイ. [Thesis]. Nara Institute of Science and Technology / 奈良先端科学技術大学院大学; Available from: http://hdl.handle.net/10061/2831

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.

Case Western Reserve University

10. Wan, Youzhong. THE FUNCTION OF INTERLEUKIN-1 RECEPTOR ASSOCIATED KINASE 2 IN TOLL-LIKE RECEPTOR-MEDIATED SIGNALING.

Degree: PhD, Genetics, 2010, Case Western Reserve University

URL: http://rave.ohiolink.edu/etdc/view?acc_num=case1278430683

► Toll-like receptors (TLRs), important pathogen recognition receptors that mediate innate immune responses against infections, detect the invading pathogens through pathogen associated molecular patterns, and then… (more)

▼ Toll-like receptors (TLRs), important pathogen recognition receptors that mediate innate immune responses against infections, detect the invading pathogens through pathogen associated molecular patterns, and then induce the production of proinflammatory cytokines and interferons through a variety of signaling cascades. Although proinflammatory cytokines and interferons are essential for eliminating the pathogens, aberrant activation of TLR–mediated signaling has been implicated in many autoimmune diseases and chronic inflammation. Dissecting the molecular mechanisms of TLR-mediated signaling will not only improve our understanding of innate immune responses but also provide rationales for the development of effective treatments for infectious and autoimmune diseases. The function of interleukin-1 receptor associated kinase 2 (IRAK2) in TLR-mediated signaling is investigated in this dissertation. Although IRAK2 deficiency leads to decreased production of proinflammatory cytokines in multiple TLR-mediated signaling pathways, the mechanisms involved are not all the same. In TLR4-mediated signaling, IRAK2 is required for stabilizing proinflammatory cytokine mRNAs and promoting their translation. In TLR7-mediated signaling, IRAK2 is essential for sustaining the activation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF¿B) at late times of stimulation. While IRAK2 is also essential for sustaining NF¿B activation in TLR9-mediated signaling at late times of stimulation, IRAK2 deficiency leads to increased activation of multiple signaling cascades downstream of TLR9 at early times. Strikingly, increased activation of interferon regulatory factor 7 leads to increased interferon production in IRAK2-deficient plasmacytoid dendritic cells stimulated with TLR9 ligand. Compared to signaling mediated by other TLRs, TLR9-mediated signaling is controlled by IRAK2 more tightly, most likely to prevent immune responses caused by inappropriate recognition of host DNA. The studies presented here, which have examined the function of IRAK2 in different TLR-mediated signaling pathways, can aid in the identification of new therapeutic targets and advance our understanding of innate immune responses. Advisors/Committee Members: Conlon, Ronald (Committee Chair), Stark, George (Advisor).

Subjects/Keywords: IRAK; TLR; innate immunity

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APA (6^th Edition):

Wan, Y. (2010). THE FUNCTION OF INTERLEUKIN-1 RECEPTOR ASSOCIATED KINASE 2 IN TOLL-LIKE RECEPTOR-MEDIATED SIGNALING. (Doctoral Dissertation). Case Western Reserve University. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=case1278430683

Chicago Manual of Style (16^th Edition):

Wan, Youzhong. “THE FUNCTION OF INTERLEUKIN-1 RECEPTOR ASSOCIATED KINASE 2 IN TOLL-LIKE RECEPTOR-MEDIATED SIGNALING.” 2010. Doctoral Dissertation, Case Western Reserve University. Accessed January 19, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=case1278430683.

MLA Handbook (7^th Edition):

Wan, Youzhong. “THE FUNCTION OF INTERLEUKIN-1 RECEPTOR ASSOCIATED KINASE 2 IN TOLL-LIKE RECEPTOR-MEDIATED SIGNALING.” 2010. Web. 19 Jan 2020.

Vancouver:

Wan Y. THE FUNCTION OF INTERLEUKIN-1 RECEPTOR ASSOCIATED KINASE 2 IN TOLL-LIKE RECEPTOR-MEDIATED SIGNALING. [Internet] [Doctoral dissertation]. Case Western Reserve University; 2010. [cited 2020 Jan 19]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=case1278430683.

Council of Science Editors:

Wan Y. THE FUNCTION OF INTERLEUKIN-1 RECEPTOR ASSOCIATED KINASE 2 IN TOLL-LIKE RECEPTOR-MEDIATED SIGNALING. [Doctoral Dissertation]. Case Western Reserve University; 2010. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=case1278430683

Penn State University

11. Dispenza, Melanie Claire. IMMUNOMODULATORY EFFECTS OF ISOTRETINOIN IN VIVO.

Degree: PhD, Physiology, 2011, Penn State University

URL: https://etda.libraries.psu.edu/catalog/11965

► Acne is a common human ailment that can cause significant physical and psychological morbidity. Though it is thought to be partially caused by Propionibacterium acnes… (more)

Subjects/Keywords: monocytes; innate immunity; acne

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APA (6^th Edition):

Dispenza, M. C. (2011). IMMUNOMODULATORY EFFECTS OF ISOTRETINOIN IN VIVO. (Doctoral Dissertation). Penn State University. Retrieved from https://etda.libraries.psu.edu/catalog/11965

Chicago Manual of Style (16^th Edition):

Dispenza, Melanie Claire. “IMMUNOMODULATORY EFFECTS OF ISOTRETINOIN IN VIVO.” 2011. Doctoral Dissertation, Penn State University. Accessed January 19, 2020. https://etda.libraries.psu.edu/catalog/11965.

MLA Handbook (7^th Edition):

Dispenza, Melanie Claire. “IMMUNOMODULATORY EFFECTS OF ISOTRETINOIN IN VIVO.” 2011. Web. 19 Jan 2020.

Vancouver:

Dispenza MC. IMMUNOMODULATORY EFFECTS OF ISOTRETINOIN IN VIVO. [Internet] [Doctoral dissertation]. Penn State University; 2011. [cited 2020 Jan 19]. Available from: https://etda.libraries.psu.edu/catalog/11965.

Council of Science Editors:

Dispenza MC. IMMUNOMODULATORY EFFECTS OF ISOTRETINOIN IN VIVO. [Doctoral Dissertation]. Penn State University; 2011. Available from: https://etda.libraries.psu.edu/catalog/11965

Louisiana State University

12. Guo, Xunyang. RNAi-mediated Antiviral Immunity in Caenorhabditis elegans.

Degree: PhD, 2013, Louisiana State University

URL: etd-11082013-124052 ; https://digitalcommons.lsu.edu/gradschool_dissertations/3132

► Viruses are tiny intracellular parasites that often cause devastating diseases on cellular organisms. To suppress viral infection, cellular organisms have evolved a wide spectrum of… (more)

▼ Viruses are tiny intracellular parasites that often cause devastating diseases on cellular organisms. To suppress viral infection, cellular organisms have evolved a wide spectrum of antiviral defense mechanisms. Antiviral RNA interference (RNAi) is one of the antiviral mechanisms conserved in eukaryotes. During antiviral RNAi, the destruction of invading viral RNAs is mediated by small interfering RNAs derived from the viral replication complex, in the form of double-stranded RNA (dsRNA). Because of its sequence-specific nature, antiviral RNAi can also target host homologous transcripts, for instance leading to disease syndromes in plants. As a counter-defense mechanism, many viruses produce RNAi suppressors that suppress RNAi through distinct mechanisms. So far, RNAi-mediated virus-host interactions have remained largely unexplored in the nematode worms which are known to have a unique RNAi gene constitution. As a result, whether virus-derived siRNAs (viRNAs) are able to direct worm gene silencing, whether heterologous viral suppressors are still functional in nematode worms and how the worm-specific RNAi genes contribute to antiviral RNAi remain open questions. In this thesis I describe my exploration of several aspects of RNAi-mediated virus-host interaction in the nematode Caenorhabditis elegans. Through the study of virus-induced gene silencing in C. elegans I found that viRNAs can target and silence host genes. This is the first demonstration that viRNAs have the potential to silence host gene expression in the animal kingdom. Since certain viral suppressors that inhibit viRNA function without a size reference become resistant to RNAi but some suppressors that specifically suppress the function of 21-nucleotide (nt) viRNAs still sensitive to RNAi, I conclude that 21-nt viRNAs do not play a major role in worm antiviral RNAi. My study on the function of a worm-specific RNAi gene, called rsd-2 (RNAi spreading defective 2), suggested that antiviral RNAi in C. elegans can be initiated in the absence of a dsRNA binding protein, which is in sharp contrast to that in plant and insect systems. Through functional domain swap and viRNA profiling, I found that RIG-I-like RNA helicases contribute to worm antiviral RNAi through distinct mechanisms with one of them contributing to virus detection.

Subjects/Keywords: RNAi; innate immunity; C.elegans

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APA (6^th Edition):

Guo, X. (2013). RNAi-mediated Antiviral Immunity in Caenorhabditis elegans. (Doctoral Dissertation). Louisiana State University. Retrieved from etd-11082013-124052 ; https://digitalcommons.lsu.edu/gradschool_dissertations/3132

Chicago Manual of Style (16^th Edition):

Guo, Xunyang. “RNAi-mediated Antiviral Immunity in Caenorhabditis elegans.” 2013. Doctoral Dissertation, Louisiana State University. Accessed January 19, 2020. etd-11082013-124052 ; https://digitalcommons.lsu.edu/gradschool_dissertations/3132.

MLA Handbook (7^th Edition):

Guo, Xunyang. “RNAi-mediated Antiviral Immunity in Caenorhabditis elegans.” 2013. Web. 19 Jan 2020.

Vancouver:

Guo X. RNAi-mediated Antiviral Immunity in Caenorhabditis elegans. [Internet] [Doctoral dissertation]. Louisiana State University; 2013. [cited 2020 Jan 19]. Available from: etd-11082013-124052 ; https://digitalcommons.lsu.edu/gradschool_dissertations/3132.

Council of Science Editors:

Guo X. RNAi-mediated Antiviral Immunity in Caenorhabditis elegans. [Doctoral Dissertation]. Louisiana State University; 2013. Available from: etd-11082013-124052 ; https://digitalcommons.lsu.edu/gradschool_dissertations/3132

University of Miami

13. Ma, Zhe. DDX24 Negatively Regulates Cytosolic RNA Mediated Innate Immune Signaling.

Degree: PhD, Cancer Biology (Medicine), 2013, University of Miami

URL: https://scholarlyrepository.miami.edu/oa_dissertations/1098

► Innate immunity is characterized by production of type I interferon which is necessary for the stimulation of effective anti-viral host defense. Upon recognition of cytosol… (more)

Subjects/Keywords: Innate immunity: RIG-I

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APA (6^th Edition):

Ma, Z. (2013). DDX24 Negatively Regulates Cytosolic RNA Mediated Innate Immune Signaling. (Doctoral Dissertation). University of Miami. Retrieved from https://scholarlyrepository.miami.edu/oa_dissertations/1098

Chicago Manual of Style (16^th Edition):

Ma, Zhe. “DDX24 Negatively Regulates Cytosolic RNA Mediated Innate Immune Signaling.” 2013. Doctoral Dissertation, University of Miami. Accessed January 19, 2020. https://scholarlyrepository.miami.edu/oa_dissertations/1098.

MLA Handbook (7^th Edition):

Ma, Zhe. “DDX24 Negatively Regulates Cytosolic RNA Mediated Innate Immune Signaling.” 2013. Web. 19 Jan 2020.

Vancouver:

Ma Z. DDX24 Negatively Regulates Cytosolic RNA Mediated Innate Immune Signaling. [Internet] [Doctoral dissertation]. University of Miami; 2013. [cited 2020 Jan 19]. Available from: https://scholarlyrepository.miami.edu/oa_dissertations/1098.

Council of Science Editors:

Ma Z. DDX24 Negatively Regulates Cytosolic RNA Mediated Innate Immune Signaling. [Doctoral Dissertation]. University of Miami; 2013. Available from: https://scholarlyrepository.miami.edu/oa_dissertations/1098

University of Kentucky

14. Banerjee, Meenakshi. PLATELET ENDOCYTOSIS: ROLES IN HEMOSTASIS AND INNATE IMMUNITY.

Degree: 2017, University of Kentucky

URL: https://uknowledge.uky.edu/biochem_etds/32

► Endocytosis is key to fibrinogen (Fg) uptake, receptor trafficking of integrins (αIIbβ3, αvβ3) and purinergic receptors (P2Y1, P2Y12), and thereby for normal platelet function. However,… (more)

▼ Endocytosis is key to fibrinogen (Fg) uptake, receptor trafficking of integrins (αIIbβ3, αvβ3) and purinergic receptors (P2Y1, P2Y12), and thereby for normal platelet function. However, platelet endocytosis could potentially be critical for actively sensing changes in vascular micro-environments and responding accordingly to what is being taken up. This is a more dynamic view of platelets as active surveyors of the vasculature; extending the importance of platelet endocytosis beyond granule biogenesis and perhaps even hemostasis. The mechanistic underpinnings of endocytosis, its importance in platelets, and the molecular machinery required and possible trafficking routes are however understudied, in part due to a lack of experimental tools. The work presented here, puts forth new players that regulate platelet endocytosis and mediate cargo loading and hemostasis as well as provides a novel mechanistic understanding of how endocytosis allows platelets to act as immune cells and become the first responders to pathogens in the vasculature. Previously we showed the importance of ADP-ribosylation factor 6 (Arf6), which regulates αIIbβ3-mediated Fg uptake/storage and affects acute platelet functions e.g., clot retraction and spreading. To further identify elements of this endocytic machinery, we examined the role of a vesicle-residing Soluble N-ethylmaleimide Factor Attachment Protein Receptor (v-SNARE) called Cellubrevin/Vesicle Associated Membrane Protein-3 (VAMP-3) in platelet function. VAMP-3 KO mice had less platelet-associated Fg, indicating a defect in Fg uptake/storage. Loss of VAMP-3 led to defective uptake of fluorescently-tagged Fg and low-molecular dextran in platelets though it had a greater negative effect on receptor-mediated Fg uptake than on the fluid-phase marker uptake. Additionally, we followed the time-dependent trafficking of Fg and dextran into platelets using 3D-Structured Illumination Microscopy. Wild-type platelets endocytosed both cargo but quickly sorted them into distinct compartments with partial overlap occurring only at early time points. Sorting was unaffected in VAMP-3KO platelets. VAMP-3 loss did affect some acute platelet functions leading to enhanced spreading on Fg and faster clot retraction compared to wild-type. Additionally, the rate of JAK2 phosphorylation, initiated through the thrombopoietin receptor (TPOR/Mpl) activation, was affected in VAMP-3 KO platelets. The idea that platelets can act as immune cells and contribute to innate immunity has been increasingly gaining ground. Groups have correlated thrombocytopenia with clinical outcomes of viremia and bacteremia. Chronic viral infections, e.g., HIV-1, severely increase the risk of acute myocardial infarction (MI), possibly via some level of platelet activation, contributing to increased thrombotic potential. Platelets do endocytose viruses and bacteria, but the molecular machinery is ill-defined. In nucleated cells, responses to HIV-1 are mediated by virus phagocytosis/endocytosis, degradation to release Toll-like Receptor…

Subjects/Keywords: platelets; endocytosis; innate immunity; Biochemistry

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Banerjee, M. (2017). PLATELET ENDOCYTOSIS: ROLES IN HEMOSTASIS AND INNATE IMMUNITY. (Doctoral Dissertation). University of Kentucky. Retrieved from https://uknowledge.uky.edu/biochem_etds/32

Chicago Manual of Style (16^th Edition):

Banerjee, Meenakshi. “PLATELET ENDOCYTOSIS: ROLES IN HEMOSTASIS AND INNATE IMMUNITY.” 2017. Doctoral Dissertation, University of Kentucky. Accessed January 19, 2020. https://uknowledge.uky.edu/biochem_etds/32.

MLA Handbook (7^th Edition):

Banerjee, Meenakshi. “PLATELET ENDOCYTOSIS: ROLES IN HEMOSTASIS AND INNATE IMMUNITY.” 2017. Web. 19 Jan 2020.

Vancouver:

Banerjee M. PLATELET ENDOCYTOSIS: ROLES IN HEMOSTASIS AND INNATE IMMUNITY. [Internet] [Doctoral dissertation]. University of Kentucky; 2017. [cited 2020 Jan 19]. Available from: https://uknowledge.uky.edu/biochem_etds/32.

Council of Science Editors:

Banerjee M. PLATELET ENDOCYTOSIS: ROLES IN HEMOSTASIS AND INNATE IMMUNITY. [Doctoral Dissertation]. University of Kentucky; 2017. Available from: https://uknowledge.uky.edu/biochem_etds/32

University of Manitoba

15. Dick, Kevin James. Mutational analysis of the dsRNA binding domain of Vaccinia Virus E3 protein.

Degree: Medical Microbiology, 2011, University of Manitoba

URL: http://hdl.handle.net/1993/4852

► Vaccinia virus E3 protein is known to bind double-stranded RNA and mediate interferon resistance. Alanine scanning mutagenesis was performed on its dsRNA binding domain, sufficient… (more)

Subjects/Keywords: Virology; Innate Immunity; Poxvirus

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APA (6^th Edition):

Dick, K. J. (2011). Mutational analysis of the dsRNA binding domain of Vaccinia Virus E3 protein. (Masters Thesis). University of Manitoba. Retrieved from http://hdl.handle.net/1993/4852

Chicago Manual of Style (16^th Edition):

Dick, Kevin James. “Mutational analysis of the dsRNA binding domain of Vaccinia Virus E3 protein.” 2011. Masters Thesis, University of Manitoba. Accessed January 19, 2020. http://hdl.handle.net/1993/4852.

MLA Handbook (7^th Edition):

Dick, Kevin James. “Mutational analysis of the dsRNA binding domain of Vaccinia Virus E3 protein.” 2011. Web. 19 Jan 2020.

Vancouver:

Dick KJ. Mutational analysis of the dsRNA binding domain of Vaccinia Virus E3 protein. [Internet] [Masters thesis]. University of Manitoba; 2011. [cited 2020 Jan 19]. Available from: http://hdl.handle.net/1993/4852.

Council of Science Editors:

Dick KJ. Mutational analysis of the dsRNA binding domain of Vaccinia Virus E3 protein. [Masters Thesis]. University of Manitoba; 2011. Available from: http://hdl.handle.net/1993/4852

University of Texas Southwestern Medical Center

16. Owen, David Matthew. Hepatitis C Virus Entry into Hepatocytes and Engagement of Innate Immune Defenses.

Degree: 2011, University of Texas Southwestern Medical Center

URL: http://hdl.handle.net/2152.5/874

► Hepatitis C virus (HCV) infection is a major cause of liver disease and a global health problem with inadequate treatment options. An improved understanding of… (more)

▼ Hepatitis C virus (HCV) infection is a major cause of liver disease and a global health problem with inadequate treatment options. An improved understanding of how HCV exploits and subverts host factors to establish infection should yield potential targets for therapy. This study uses a recently developed cell culture model of HCV infection to examine HCV entry and engagement of innate immune defenses. HCV associates with host apolipoproteins and enters hepatocytes through complex processes involving some combination of CD81, claudin-I, occludin, and scavenger receptor BI. Here I show that HCV forms a complex with very low density lipoprotein (VLDL) within infected hepatocytes and uses this association to support infection through the low density lipoprotein receptor (LDL-R). Blocking experiments demonstrate that beta-VLDL and apolipoprotein E (apoE) can compete with HCV for entry. Knockdown of the LDL-R by treatment with 25-hydroxycholesterol or siRNA ablated ligand uptake and reduced HCV infection of cells, whereas infection was rescued upon cell ectopic LDL-R expression. Analyses of gradient-fractionated HCV demonstrate that apoE is associated with HCV virions exhibiting peak infectivity and dependence upon the LDL-R for cell entry. These results define the LDL-R as a cooperative HCV co-receptor that supports viral entry and infectivity through interaction with apoE ligand present in an infectious HCV/lipoprotein complex comprising the virion. Furthermore, upon entry HCV induces an initial transient activation of interferon regulatory factor-3 (IRF3) which is dependent on retinoic acid inducible gene I (RIG-I) and interferon-beta promoter stimulator-1 (IPS-1). This activation produces an antiviral activity which inhibits HCV entry and replication. HCV NS3/4A protease activity blocks this activation within 48 hours. At later time points post infection HCV activates NF-kappaB in a RIG-I independent manner leading to inflammatory cytokine production. These studies identify 3 potential targets for future HCV therapy: 1) alteration of HCV-lipoprotein interaction to disrupt entry, 2) blockade of NS3/4A protease activity to restore innate antiviral response, and 3) modulation of HCV induced NF-kappaB signaling to downregulate chronic inflammation. Advisors/Committee Members: Gale, Michael, Jr..

Subjects/Keywords: RNA Helicases; Immunity, Innate; Hepacivirus

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APA (6^th Edition):

Owen, D. M. (2011). Hepatitis C Virus Entry into Hepatocytes and Engagement of Innate Immune Defenses. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/874

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Owen, David Matthew. “Hepatitis C Virus Entry into Hepatocytes and Engagement of Innate Immune Defenses.” 2011. Thesis, University of Texas Southwestern Medical Center. Accessed January 19, 2020. http://hdl.handle.net/2152.5/874.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Owen, David Matthew. “Hepatitis C Virus Entry into Hepatocytes and Engagement of Innate Immune Defenses.” 2011. Web. 19 Jan 2020.

Vancouver:

Owen DM. Hepatitis C Virus Entry into Hepatocytes and Engagement of Innate Immune Defenses. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2011. [cited 2020 Jan 19]. Available from: http://hdl.handle.net/2152.5/874.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Owen DM. Hepatitis C Virus Entry into Hepatocytes and Engagement of Innate Immune Defenses. [Thesis]. University of Texas Southwestern Medical Center; 2011. Available from: http://hdl.handle.net/2152.5/874

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Guelph

17. Misk, Ehab. Pathogenesis and Distribution of Spring Viremia of Carp Virus (SVCV) in Ontario .

Degree: 2016, University of Guelph

URL: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/9687

► Spring viremia of carp virus (SVCV), an OIE reportable rhabdovirus and fish pathogen, was identified in Canada in 2006 in Hamilton Harbour but has not… (more)

▼ Spring viremia of carp virus (SVCV), an OIE reportable rhabdovirus and fish pathogen, was identified in Canada in 2006 in Hamilton Harbour but has not been reported subsequently. SVCV can have a significant impact on cyprinids, and so the susceptibility of three baitfish species (emerald shiner Notropis atherinoides, fathead minnow Pimpheles promelas, white sucker Catostomus commersonii from the order Cypriniformes was assessed using experimental infection. Millions of baitfish are moved around the province to support the sports fishing industry, and this represents a risk for spread of the virus. Emerald shiner, fathead minnow and koi (43, 53, and 33% mortality, respectively) were highly susceptible, but white sucker or rainbow trout (12.5 and 0% mortality), were not. Infection was confirmed by virus isolation and RT-qPCR and SVCV was immunolocalized in association with histological lesions using immunohistochemistry. A one-step reverse transcription quantitative PCR (RT-qPCR) was adapted and used retrospectively to test samples collected by the Ontario Ministry of Natural Resources for surveillance from 2008 to 2012. A total of 1432 fish from 35 water bodies in Ontario were examined using RT-qPCR, but no additional fish were identified with SVCV. Finally, the pathogenesis of the Rhabdovirus-host interaction at the gill epithelium was investigated using the RTgill-W1 cells. The cell line was pretreated with UV-inactivated (killed) VHSV and recombinant FliC and then infected with viral hemorrhagic septicemia virus (VHSV). The viral load and gene expression was investigated 1, 3, and 6 d post infection (PI) with qPCR. In addition, the transcriptome response of RTgill-W1 cells at 36 h post-treatment with SVCV, VHSV, UV-inactivated VHSV and FliC were tested using microarray and RT-qPCR. Pretreatment of RTgill-W1 cells with killed VSHV induced a reduction in viral load (nucleoprotein copy number by RT-qPCR) after infection. Transcription profiles in VHSV- and SVCV-infected or killed VHSV and FliC pretreated RTgill-W1 cells 36 h post-exposure detected 24, 22, 123 and 190 differentially expressed probes, which contained several important gene candidates with a potentially key role in innate immunity to rhabdovirus infection in gill epithelium. Advisors/Committee Members: Lumsden, John (advisor).

Subjects/Keywords: Innate immunity; SVCV; Microarray

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APA (6^th Edition):

Misk, E. (2016). Pathogenesis and Distribution of Spring Viremia of Carp Virus (SVCV) in Ontario . (Thesis). University of Guelph. Retrieved from https://atrium.lib.uoguelph.ca/xmlui/handle/10214/9687

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Misk, Ehab. “Pathogenesis and Distribution of Spring Viremia of Carp Virus (SVCV) in Ontario .” 2016. Thesis, University of Guelph. Accessed January 19, 2020. https://atrium.lib.uoguelph.ca/xmlui/handle/10214/9687.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Misk, Ehab. “Pathogenesis and Distribution of Spring Viremia of Carp Virus (SVCV) in Ontario .” 2016. Web. 19 Jan 2020.

Vancouver:

Misk E. Pathogenesis and Distribution of Spring Viremia of Carp Virus (SVCV) in Ontario . [Internet] [Thesis]. University of Guelph; 2016. [cited 2020 Jan 19]. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/9687.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Misk E. Pathogenesis and Distribution of Spring Viremia of Carp Virus (SVCV) in Ontario . [Thesis]. University of Guelph; 2016. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/9687

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Guelph

18. Berghuis, Lesley. Stimulating innate immunity in feedlot cattle: strategies to induce tracheal antimicrobial peptide gene expression .

Degree: 2014, University of Guelph

URL: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/7762

► Tracheal antimicrobial peptide (TAP) is a β-defensin with microbicidal activity against bacterial pathogens causing bovine respiratory disease. Lipopolysaccharide stimulates TAP gene expression, with maximal effect… (more)

Subjects/Keywords: Innate immunity; feedlot cattle

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APA (6^th Edition):

Berghuis, L. (2014). Stimulating innate immunity in feedlot cattle: strategies to induce tracheal antimicrobial peptide gene expression . (Thesis). University of Guelph. Retrieved from https://atrium.lib.uoguelph.ca/xmlui/handle/10214/7762

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Berghuis, Lesley. “Stimulating innate immunity in feedlot cattle: strategies to induce tracheal antimicrobial peptide gene expression .” 2014. Thesis, University of Guelph. Accessed January 19, 2020. https://atrium.lib.uoguelph.ca/xmlui/handle/10214/7762.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Berghuis, Lesley. “Stimulating innate immunity in feedlot cattle: strategies to induce tracheal antimicrobial peptide gene expression .” 2014. Web. 19 Jan 2020.

Vancouver:

Berghuis L. Stimulating innate immunity in feedlot cattle: strategies to induce tracheal antimicrobial peptide gene expression . [Internet] [Thesis]. University of Guelph; 2014. [cited 2020 Jan 19]. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/7762.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Berghuis L. Stimulating innate immunity in feedlot cattle: strategies to induce tracheal antimicrobial peptide gene expression . [Thesis]. University of Guelph; 2014. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/7762

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Saskatchewan

19. Magiri, Royford Bundi 1983-. INNATE IMMUNE RESPONSES ACTIVATED BY THE ADJUVANT POLY [DI (SODIUM CARBOXYLATOETHYLPHENOXY)PHOSPHAZENE](PCEP) IN PIGS.

Degree: 2019, University of Saskatchewan

URL: http://hdl.handle.net/10388/12208

► ABSTRACT Adjuvants are critical components of vaccines because they enhance antigen-specific immune responses to protect against disease. However, the mechanisms of action (MOA) of most… (more)

▼ ABSTRACT Adjuvants are critical components of vaccines because they enhance antigen-specific immune responses to protect against disease. However, the mechanisms of action (MOA) of most adjuvants are not well understood and they particularly are under-investigated in large animal species including pigs and cattle. This knowledge gap may limit our ability to design effective vaccines for livestock. Understanding the mechanisms by which adjuvants mediate their effects could provide critical information on how innate immunity influences the development of adaptive immunity. Furthermore, knowledge on the MOA of adjuvants may inform vaccine the safety. In the present investigations, we studied the MOA of the experimental adjuvant polydi(sodium carboxylatoethylphenoxy)phosphazene (PCEP) in pigs. First, we administered PCEP by intradermal (i.d.) injection into pigs and assessed its impact on the expression of select immune response genes known as ‘adjuvant response genes’ over time. We observed that PCEP induced the expression of chemokine (C-C motif) ligand 2 (CCL-2), proinflammatory cytokine interleukin (IL)-6, IL-13 and macrophage scavenger receptor 1 (MSR1) genes at the site of injection. Next, we evaluated whether these gene expressions translate to protein transcription by accessing local and systemic production of cytokines after intradermal injection of PCEP into piglets and whether the cytokines produced induces recruitment of immune cells at the site of injection and in the draining lymph nodes. We observed that, at the site of injection, PCEP induced increased production of IL-1β and IL-13 cytokines, increased cellular infiltration of macrophages, T and B cells, and other leucocytes especially neutrophils as well as showing necrotic debris which might cause release of damage associated molecular patterns (DAMPs) and activate the inflammasome. In the draining lymph nodes, the cytokines IL-1β and IL-6 were elevated and there was increased leucocyte infiltration. No changes in cytokine levels were detected in the blood after PCEP injection indicating that the immunostimulatory effect of PCEP is local but not systemic. Because i.d. injection of PCEP induced signs of necrosis (cell death), we investigated whether reduction of the adjuvant dose reduced tissue damage without negatively impacting antigen-specific immune responses. We conducted two studies to address this issue. In the first study, we injected piglets i.d with varying doses of PCEP alone as follows: 500 μg, 100 μg, or 20 μg PCEP into piglets and evaluated the inflammatory responses. The four parameters evaluated were granuloma formation, lymphocytic infiltration, necrosis, and suppurative inflammation at the injection site and the draining lymph nodes over 14 days. When PCEP was injected alone, we observed that only 500 μg consistently induced significant necrosis and suppurative inflammation. However, the medium dose (100 μg) PCEP did induce significant skin granulomas and lymphocyte infiltration, where as the only significant response induced in… Advisors/Committee Members: Mutwiri, George, Wilson, Heather, Tikoo, Suresh, Huang, Yanyun, Singh, Baljit, Gomis, Susantha.

Subjects/Keywords: Innate immunity and adjuvants

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Magiri, R. B. 1. (2019). INNATE IMMUNE RESPONSES ACTIVATED BY THE ADJUVANT POLY [DI (SODIUM CARBOXYLATOETHYLPHENOXY)PHOSPHAZENE](PCEP) IN PIGS. (Thesis). University of Saskatchewan. Retrieved from http://hdl.handle.net/10388/12208

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Magiri, Royford Bundi 1983-. “INNATE IMMUNE RESPONSES ACTIVATED BY THE ADJUVANT POLY [DI (SODIUM CARBOXYLATOETHYLPHENOXY)PHOSPHAZENE](PCEP) IN PIGS.” 2019. Thesis, University of Saskatchewan. Accessed January 19, 2020. http://hdl.handle.net/10388/12208.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Magiri, Royford Bundi 1983-. “INNATE IMMUNE RESPONSES ACTIVATED BY THE ADJUVANT POLY [DI (SODIUM CARBOXYLATOETHYLPHENOXY)PHOSPHAZENE](PCEP) IN PIGS.” 2019. Web. 19 Jan 2020.

Vancouver:

Magiri RB1. INNATE IMMUNE RESPONSES ACTIVATED BY THE ADJUVANT POLY [DI (SODIUM CARBOXYLATOETHYLPHENOXY)PHOSPHAZENE](PCEP) IN PIGS. [Internet] [Thesis]. University of Saskatchewan; 2019. [cited 2020 Jan 19]. Available from: http://hdl.handle.net/10388/12208.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Magiri RB1. INNATE IMMUNE RESPONSES ACTIVATED BY THE ADJUVANT POLY [DI (SODIUM CARBOXYLATOETHYLPHENOXY)PHOSPHAZENE](PCEP) IN PIGS. [Thesis]. University of Saskatchewan; 2019. Available from: http://hdl.handle.net/10388/12208

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Illinois – Urbana-Champaign

20. Granger, Kyle L. A pilot study on the effects of sow management practices on piglet immune responsiveness to weaning stress.

Degree: MS, Animal Sciences, 2016, University of Illinois – Urbana-Champaign

URL: http://hdl.handle.net/2142/95266

► The consequences of maternal prenatal stress exposure of the gestating sow on the developing immune system of her offspring is not well understood. There is… (more)

▼ The consequences of maternal prenatal stress exposure of the gestating sow on the developing immune system of her offspring is not well understood. There is limited data that primarily focuses on the health and well-being of the neonates of livestock animals, principally within the swine industry, in relation to the presence of unavoidable production stressors, including—but not limited to—weaning, mixing and social hierarchy. Each of the aforementioned stressors has been previously shown to affect the health, well-being, performance and productivity of sows as well as exacerbate the disease process by compromising the immune system. Thus, more information is needed to elucidate the complex relationship between prenatal stressors and postnatal immunological competence of the offspring. The objective of this thesis was to assess the effects of sow housing environment, social stress, and dietary fiber treatments during gestation on the immune and stress responsiveness of their progeny to weaning stress. Piglets were obtained from a larger-scale study of a 180 group-housed gestating sows. Briefly, sows were randomly allotted to 1 of 2 high fiber gestation diets (1) 30% wheat middlings and 15% soybean hulls (MID-SOY) or 30% distillers dried grains and 30% corn germ meal (DDG-GM) and to a group pen with feeding stalls of either 0.6 m (SHT) or 1.8 m (LNG) in length. Sows were fed dietary treatments starting on gestational d 35 and then moved to treatment pens at gestational d 37 and kept until d 104. On d 37, prior to moving into their experimental pens, a subsample of sows were subjected to a dominance test by which we determined a dominance value (DV). Those sows with a high DV were labeled dominant (DOM) and those with a low DV were labeled submissive (SUB). From both the larger study and the subsample of sows, 40-42 piglets were selected (balanced across treatments) based on body weight prior to weaning, with the two heaviest and two lightest piglets from each litter being used. All piglets were weaned at 19 ± 2 d-of-age. Blood samples were taken 24h prior to weaning, and then 7 and 14 days post-weaning to assess descriptive and functional aspects of both innate and adaptive immunity and cortisol. These data revealed that piglets weaned from sows fed MID-SOY during gestation had a profile indicative of a skewed TH1 (cell-mediated) response, while piglets weaned from sows fed DDG-GM diet were skewed toward TH2 (humoral) response. Piglets from sows housed in pens with LNG feeding stalls were better able to cope with weaning stress compared to those piglets from sows housed in pens with SHT. Moreover, sow social status differentially impact piglet immune responsiveness to weaning stress. Piglets weaned from SUB sows had a greater cell-mediated immune response which may have cost them in terms of performance because piglets from DOM sows had improved performance. These results show that: (1) feeding gestating sows high fiber diets can impact the development and growth of her offspring; (2) physical environment of gestating… Advisors/Committee Members: Salak-Johnson, Janeen L (advisor), Gaskins, Rex (committee member), Dailey, Megan J (committee member).

Subjects/Keywords: adaptive immunity; gestation; innate immunity; piglet; weaning

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APA (6^th Edition):

Granger, K. L. (2016). A pilot study on the effects of sow management practices on piglet immune responsiveness to weaning stress. (Thesis). University of Illinois – Urbana-Champaign. Retrieved from http://hdl.handle.net/2142/95266

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Granger, Kyle L. “A pilot study on the effects of sow management practices on piglet immune responsiveness to weaning stress.” 2016. Thesis, University of Illinois – Urbana-Champaign. Accessed January 19, 2020. http://hdl.handle.net/2142/95266.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Granger, Kyle L. “A pilot study on the effects of sow management practices on piglet immune responsiveness to weaning stress.” 2016. Web. 19 Jan 2020.

Vancouver:

Granger KL. A pilot study on the effects of sow management practices on piglet immune responsiveness to weaning stress. [Internet] [Thesis]. University of Illinois – Urbana-Champaign; 2016. [cited 2020 Jan 19]. Available from: http://hdl.handle.net/2142/95266.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Granger KL. A pilot study on the effects of sow management practices on piglet immune responsiveness to weaning stress. [Thesis]. University of Illinois – Urbana-Champaign; 2016. Available from: http://hdl.handle.net/2142/95266

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Dalhousie University

21. Moore, Jill Alexandra. Implications of the Innate Immune Response in Tuberculosis and Cardiac Allograft Vasculopathy.

Degree: MS, Department of Pathology, 2014, Dalhousie University

URL: http://hdl.handle.net/10222/53157

► Reactivation of latent tuberculosis (TB) in HIV-infected individuals has arisen as a major contributor to early death in areas where TB and HIV overlap. CD4+… (more)

Subjects/Keywords: innate immunity, macrophages, tuberculosis; innate immunity, macrophages, atherosclerosis, cardiac transplantation

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APA (6^th Edition):

Moore, J. A. (2014). Implications of the Innate Immune Response in Tuberculosis and Cardiac Allograft Vasculopathy. (Masters Thesis). Dalhousie University. Retrieved from http://hdl.handle.net/10222/53157

Chicago Manual of Style (16^th Edition):

Moore, Jill Alexandra. “Implications of the Innate Immune Response in Tuberculosis and Cardiac Allograft Vasculopathy.” 2014. Masters Thesis, Dalhousie University. Accessed January 19, 2020. http://hdl.handle.net/10222/53157.

MLA Handbook (7^th Edition):

Moore, Jill Alexandra. “Implications of the Innate Immune Response in Tuberculosis and Cardiac Allograft Vasculopathy.” 2014. Web. 19 Jan 2020.

Vancouver:

Moore JA. Implications of the Innate Immune Response in Tuberculosis and Cardiac Allograft Vasculopathy. [Internet] [Masters thesis]. Dalhousie University; 2014. [cited 2020 Jan 19]. Available from: http://hdl.handle.net/10222/53157.

Council of Science Editors:

Moore JA. Implications of the Innate Immune Response in Tuberculosis and Cardiac Allograft Vasculopathy. [Masters Thesis]. Dalhousie University; 2014. Available from: http://hdl.handle.net/10222/53157

Colorado State University

22. Bickett, Thomas. T cell independent mechanisms for protection against Mycobacterium tuberculosis infection.

Degree: PhD, Cell and Molecular Biology, 2019, Colorado State University

URL: http://hdl.handle.net/10217/197402

► The live attenuated Mycobacterium bovis strain Bacille Calmette Guérin (BCG) is a potent innate immune stimulator. Innate Immunity provides the host with the ability to… (more)

Subjects/Keywords: Innate Immunity; Trained Innate Immunity; BCG; tuberculosis; Macrophage

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APA (6^th Edition):

Bickett, T. (2019). T cell independent mechanisms for protection against Mycobacterium tuberculosis infection. (Doctoral Dissertation). Colorado State University. Retrieved from http://hdl.handle.net/10217/197402

Chicago Manual of Style (16^th Edition):

Bickett, Thomas. “T cell independent mechanisms for protection against Mycobacterium tuberculosis infection.” 2019. Doctoral Dissertation, Colorado State University. Accessed January 19, 2020. http://hdl.handle.net/10217/197402.

MLA Handbook (7^th Edition):

Bickett, Thomas. “T cell independent mechanisms for protection against Mycobacterium tuberculosis infection.” 2019. Web. 19 Jan 2020.

Vancouver:

Bickett T. T cell independent mechanisms for protection against Mycobacterium tuberculosis infection. [Internet] [Doctoral dissertation]. Colorado State University; 2019. [cited 2020 Jan 19]. Available from: http://hdl.handle.net/10217/197402.

Council of Science Editors:

Bickett T. T cell independent mechanisms for protection against Mycobacterium tuberculosis infection. [Doctoral Dissertation]. Colorado State University; 2019. Available from: http://hdl.handle.net/10217/197402

23. Schrum, Jacob E. Pathways Involved in Recognition and Induction of Trained Innate Immunity by Plasmodium falciparum.

Degree: PhD, Department of Medicine, Division of Infectious Diseases and Immunology, 2017, U of Massachusetts : Med

URL: http://escholarship.umassmed.edu/gsbs_diss/917

► Malarial infection in naïve individuals induces a robust innate immune response, but our understanding of the mechanisms by which the innate immune system recognizes… (more)

Subjects/Keywords: Plasmodium falciparum; innate immunity; innate immune memory; cGAS; trained immunity; Immunity; Immunology of Infectious Disease

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APA (6^th Edition):

Schrum, J. E. (2017). Pathways Involved in Recognition and Induction of Trained Innate Immunity by Plasmodium falciparum. (Doctoral Dissertation). U of Massachusetts : Med. Retrieved from http://escholarship.umassmed.edu/gsbs_diss/917

Chicago Manual of Style (16^th Edition):

Schrum, Jacob E. “Pathways Involved in Recognition and Induction of Trained Innate Immunity by Plasmodium falciparum.” 2017. Doctoral Dissertation, U of Massachusetts : Med. Accessed January 19, 2020. http://escholarship.umassmed.edu/gsbs_diss/917.

MLA Handbook (7^th Edition):

Schrum, Jacob E. “Pathways Involved in Recognition and Induction of Trained Innate Immunity by Plasmodium falciparum.” 2017. Web. 19 Jan 2020.

Vancouver:

Schrum JE. Pathways Involved in Recognition and Induction of Trained Innate Immunity by Plasmodium falciparum. [Internet] [Doctoral dissertation]. U of Massachusetts : Med; 2017. [cited 2020 Jan 19]. Available from: http://escholarship.umassmed.edu/gsbs_diss/917.

Council of Science Editors:

Schrum JE. Pathways Involved in Recognition and Induction of Trained Innate Immunity by Plasmodium falciparum. [Doctoral Dissertation]. U of Massachusetts : Med; 2017. Available from: http://escholarship.umassmed.edu/gsbs_diss/917

24. Evans, John W., III. Itk is a Dual Action Regulator of Immunoreceptor Signaling in the Innate and Adaptive Immune System: A Dissertation.

Degree: Immunology and Microbiology, Pathology, 2013, U of Massachusetts : Med

URL: http://escholarship.umassmed.edu/gsbs_diss/688

► The cells and molecules that comprise the immune system are essential for mounting an effective response against microbes. A successful immune response limits pathology… (more)

▼ The cells and molecules that comprise the immune system are essential for mounting an effective response against microbes. A successful immune response limits pathology within the host while simultaneously eliminating the pathogen. The key to this delicate balance is the correct recognition of the pathogen and the appropriate response of immune cells. Cellular activation originates through receptors that relay information about the state of the microenvironment to different compartments within the cell. The rapid relay of information is called signal transduction and employs a network of signaling mediators such as kinases, phosphatases, adaptor molecules, and transcription factors. IL-2 inducible T cell kinase (Itk) is a non-receptor tyrosine kinase that is an integral component of signal transduction downstream of many immunoreceptors. This dissertation describes two distinct pathways that utilize Itk in both phases of the immune response. T cells use the TCR to sense a multitude of peptide-based ligands and to transmit signals inside the cell to activate cellular function. In this regard, the diversity of ligands the T cells encounter can be portrayed as analog inputs. Once a critical threshold is met, signaling events transpire in close proximity to the plasma membrane to activate major downstream pathways in the cell. The majority of these pathways are digital in nature resulting in the on or off activation of T cells. We find, however, that altering the TCR signal strength that a T cell receives can result in an analog-based response. Here, the graded expression of a transcription factor, IRF4, is modulated through the activity of Itk. We link this graded response to an NFAT-mediated pathway in which the digital vs. analog nature has been previously uncharacterized. Finally, we demonstrate that the repercussions of an analog signaling pathway is the altered expression of a second transcription factor, Eomes, which is important in the differentiation and function of T cells. These results suggest that Itk is crucial in the modulation of TCR signal strength. Mast cells primarily rely on the IgE-bound FcεR1 for pathogen recognition. Crosslinking this receptor activates mast cells and results in degranulation and cytokine production via an expansive signaling cascade. Upon stimulation, Itk is recruited to the plasma membrane and phosphorylated. Little else is known about how Itk operates inside of mast cells. We find that mast cells lacking Itk are hyperresponsive to FcεR1-mediated activation. This is most apparent in the amount of IL-4 and IL-13 produced in comparison to wild-type mast cells. Increased cytokine production was accompanied by elevated and sustained signaling downstream of the FcεR1. Finally, biochemical evidence demonstrates that Itk is part of an inhibitory complex containing the phosphatase SHIP-1. These results indicate a novel function for Itk as a negative regulator in FcεR1- mediated mast cell activation. Advisors/Committee Members: Leslie J. Berg, PhD.

Subjects/Keywords: Signal Transduction; Protein-Tyrosine Kinases; Adaptive Immunity; Innate Immunity; Immunity; Immunopathology

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APA (6^th Edition):

Evans, John W., I. (2013). Itk is a Dual Action Regulator of Immunoreceptor Signaling in the Innate and Adaptive Immune System: A Dissertation. (Doctoral Dissertation). U of Massachusetts : Med. Retrieved from http://escholarship.umassmed.edu/gsbs_diss/688

Chicago Manual of Style (16^th Edition):

Evans, John W., III. “Itk is a Dual Action Regulator of Immunoreceptor Signaling in the Innate and Adaptive Immune System: A Dissertation.” 2013. Doctoral Dissertation, U of Massachusetts : Med. Accessed January 19, 2020. http://escholarship.umassmed.edu/gsbs_diss/688.

MLA Handbook (7^th Edition):

Evans, John W., III. “Itk is a Dual Action Regulator of Immunoreceptor Signaling in the Innate and Adaptive Immune System: A Dissertation.” 2013. Web. 19 Jan 2020.

Vancouver:

Evans, John W. I. Itk is a Dual Action Regulator of Immunoreceptor Signaling in the Innate and Adaptive Immune System: A Dissertation. [Internet] [Doctoral dissertation]. U of Massachusetts : Med; 2013. [cited 2020 Jan 19]. Available from: http://escholarship.umassmed.edu/gsbs_diss/688.

Council of Science Editors:

Evans, John W. I. Itk is a Dual Action Regulator of Immunoreceptor Signaling in the Innate and Adaptive Immune System: A Dissertation. [Doctoral Dissertation]. U of Massachusetts : Med; 2013. Available from: http://escholarship.umassmed.edu/gsbs_diss/688

Universiteit Utrecht

25. Fermie, J. Failure of Immunity Against Hepatitis C Virus: Implications of Defects in Early Immunity.

Degree: 2013, Universiteit Utrecht

URL: http://dspace.library.uu.nl:8080/handle/1874/283340

► The hepatitis C virus (HCV) is an upcoming human pathogen. Although HCV infection is mostly asymptomatic, persistent infection may lead to liver failure or liver… (more)

Subjects/Keywords: HCV; Hepatitis C Virus; Adaptive immunity; Innate immunity; T cell; chronic infection; viral immunity; immunity

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APA (6^th Edition):

Fermie, J. (2013). Failure of Immunity Against Hepatitis C Virus: Implications of Defects in Early Immunity. (Masters Thesis). Universiteit Utrecht. Retrieved from http://dspace.library.uu.nl:8080/handle/1874/283340

Chicago Manual of Style (16^th Edition):

Fermie, J. “Failure of Immunity Against Hepatitis C Virus: Implications of Defects in Early Immunity.” 2013. Masters Thesis, Universiteit Utrecht. Accessed January 19, 2020. http://dspace.library.uu.nl:8080/handle/1874/283340.

MLA Handbook (7^th Edition):

Fermie, J. “Failure of Immunity Against Hepatitis C Virus: Implications of Defects in Early Immunity.” 2013. Web. 19 Jan 2020.

Vancouver:

Fermie J. Failure of Immunity Against Hepatitis C Virus: Implications of Defects in Early Immunity. [Internet] [Masters thesis]. Universiteit Utrecht; 2013. [cited 2020 Jan 19]. Available from: http://dspace.library.uu.nl:8080/handle/1874/283340.

Council of Science Editors:

Fermie J. Failure of Immunity Against Hepatitis C Virus: Implications of Defects in Early Immunity. [Masters Thesis]. Universiteit Utrecht; 2013. Available from: http://dspace.library.uu.nl:8080/handle/1874/283340

University of Alberta

26. Montgomery, Benjamin Christian Sivert. Biochemical and Functional Characterization of Inhibitory Leukocyte Immune-Type Receptors in the Channel Catfish (Ictalurus punctatus).

Degree: PhD, Department of Biological Sciences, 2012, University of Alberta

URL: https://era.library.ualberta.ca/files/37720d711

► A balance of intracellular signaling events control immune cell functions. In innate immunity, many of these signals are transmitted by subsets of cell surface proteins… (more)

▼ A balance of intracellular signaling events control immune cell functions. In innate immunity, many of these signals are transmitted by subsets of cell surface proteins known as immunoregulatory receptors. Through their recognition of a diverse array of molecules these receptors effectively translate extracellular cues into immune cell responses. These effector responses are vital for the elimination of pathogens and the destruction of damaged and/or infected host cells. In general, the ability of immunoregulatory receptors to promote or abrogate cellular responses is directly linked with their ability to transmit stimulatory and/or inhibitory signals. These signals are responsible for the direct immune cell-mediated elimination of pathogens, such as viruses and bacteria, and simultaneously protect healthy host tissue from autoimmune reactions. Co-expression of stimulatory and inhibitory immunoregulatory receptor-types by immune cells is common in all vertebrates but the majority of the research into understanding these complex networks has focused on mammals. Recently, it has been shown that immune cells in non-mammalian vertebrates, such as teleost (i.e. bony fish), express larger repertoires of immunoregulatory proteins but evidence as to how they are involved in mediating cellular signaling and controlling effector responses remain unknown. Channel catfish (Ictalurus punctatus) leukocyte immune-type receptors (IpLITRs) represent a large polymorphic gene family with members that possess the characteristics of putative stimulatory and inhibitory immunoregulatory proteins. The goal of my thesis work was to determine whether putative inhibitory IpLITR-types were bona fide functional receptors and to examine the signaling molecules/pathways involved in their activity. Using standard cellular transfection procedures, co-immunoprecipitations, site- directed mutagenesis, and adaptation of a vaccinia virus-based expression system for displaying IpLITRs on the surface of freshly isolated mouse natural killer (NK) cells, I discovered that two putative IpLITR-types, termed IpLITR1.2a and IpLITR1.1b, are both functional inhibitory receptors. I also determined that these IpLITRs effectively diminish cellular responses using two different mechanisms. Specifically, both IpLITR1.1b and IpLITR1.2a abrogated NK cell-mediated killing using ‘classical’ inhibitory tyrosine- based signaling motifs within their cytoplasmic regions, which recruited inhibitory phosphatases. Unlike IpLITR1.2a, IpLITR1.1b has additional tyrosine residues encoded within the membrane proximal region of its cytoplasmic tail that are not contained within known inhibitory motifs. Interestingly, one of these unique tyrosines abrogated the killing response of NK cells. However, unlike what I showed for IpLITR1.2a this was via a phosphatase-independent mechanism. These results highlight the conserved aspects of immunoregulatory receptor signaling in vertebrates while simultaneously revealing subtle nuances that may contribute towards a greater understanding of…

Subjects/Keywords: immunoregulatory receptors; innate immunity; Ictalurus punctatus

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APA (6^th Edition):

Montgomery, B. C. S. (2012). Biochemical and Functional Characterization of Inhibitory Leukocyte Immune-Type Receptors in the Channel Catfish (Ictalurus punctatus). (Doctoral Dissertation). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/37720d711

Chicago Manual of Style (16^th Edition):

Montgomery, Benjamin Christian Sivert. “Biochemical and Functional Characterization of Inhibitory Leukocyte Immune-Type Receptors in the Channel Catfish (Ictalurus punctatus).” 2012. Doctoral Dissertation, University of Alberta. Accessed January 19, 2020. https://era.library.ualberta.ca/files/37720d711.

MLA Handbook (7^th Edition):

Montgomery, Benjamin Christian Sivert. “Biochemical and Functional Characterization of Inhibitory Leukocyte Immune-Type Receptors in the Channel Catfish (Ictalurus punctatus).” 2012. Web. 19 Jan 2020.

Vancouver:

Montgomery BCS. Biochemical and Functional Characterization of Inhibitory Leukocyte Immune-Type Receptors in the Channel Catfish (Ictalurus punctatus). [Internet] [Doctoral dissertation]. University of Alberta; 2012. [cited 2020 Jan 19]. Available from: https://era.library.ualberta.ca/files/37720d711.

Council of Science Editors:

Montgomery BCS. Biochemical and Functional Characterization of Inhibitory Leukocyte Immune-Type Receptors in the Channel Catfish (Ictalurus punctatus). [Doctoral Dissertation]. University of Alberta; 2012. Available from: https://era.library.ualberta.ca/files/37720d711

University of Alberta

27. James, Kevin. Deciphering the mechanism(s) which limit reovirus spread in resistant lung and HNSCC cancer cells.

Degree: MS, Department of Medical Microbiology and Immunology, 2016, University of Alberta

URL: https://era.library.ualberta.ca/files/c3j333244m

► Reovirus is a naturally benign virus that preferentially replicates in transformed cells and is currently undergoing clinical trials as a promising oncolytic therapy. In normal… (more)

▼ Reovirus is a naturally benign virus that preferentially replicates in transformed cells and is currently undergoing clinical trials as a promising oncolytic therapy. In normal mouse fibroblasts, transformation by constitutively activated Ras oncogene is sufficient to promote reovirus infection. However, not all tumour cells containing Ras mutations are susceptible to reovirus, and clinical trials show mixed response to reovirus treatment. Accordingly, we aim to discover additional host-determinants important for conferring susceptibility to reovirus infection. Our first objective was to identify tumorigenic cells that restrict reovirus infection. Reovirus primary infection (at 18 hours post-infection, hpi), and dissemination over two rounds of virus replication (48 hpi) was measured in a panel of lung (H1299, A549, H23, H522, H322) and head and neck (SCC9, A253) carcinoma cells using cell-based ELISA. A549, H322, A253, and SCC9 cells were 8-90 times less permissive to reovirus dissemination relative to highly susceptible H1299 cells. Differences in cell death were observed between cells, notably in H322 and A253 cells which released up to 100-fold less progeny virions within the first 24 hpi. However, it was determined that restricted virion release was not the sole determinant for reduced reovirus cell-cell spread. We next evaluated if antiviral innate signalling contributes a barrier to reovirus dissemination among less-susceptible cells. Multiplex ELISA and qRT-PCR analysis of cell culture media and cellular RNA from reovirus-infected cells showed high levels of IFN-β, IFN-λ, and TNF- among resistant A549, H322, A253, and SCC9 cells. ShRNA-mediated knock-down of IRF3, IRF7, IFN Type I and III receptors, or IFN- neutralization in A549 cells had no effect on reovirus dissemination, suggesting that these factors are singularly insufficient to confer resistance in these cells. It remains to be determined if Type I and III IFN responses act together to promote resistance to reovirus, or if alternative antiviral pathways are involved.

Subjects/Keywords: Reovirus; Oncolytic; Cancer; Interferon; Innate Immunity; Virology

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APA (6^th Edition):

James, K. (2016). Deciphering the mechanism(s) which limit reovirus spread in resistant lung and HNSCC cancer cells. (Masters Thesis). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/c3j333244m

Chicago Manual of Style (16^th Edition):

James, Kevin. “Deciphering the mechanism(s) which limit reovirus spread in resistant lung and HNSCC cancer cells.” 2016. Masters Thesis, University of Alberta. Accessed January 19, 2020. https://era.library.ualberta.ca/files/c3j333244m.

MLA Handbook (7^th Edition):

James, Kevin. “Deciphering the mechanism(s) which limit reovirus spread in resistant lung and HNSCC cancer cells.” 2016. Web. 19 Jan 2020.

Vancouver:

James K. Deciphering the mechanism(s) which limit reovirus spread in resistant lung and HNSCC cancer cells. [Internet] [Masters thesis]. University of Alberta; 2016. [cited 2020 Jan 19]. Available from: https://era.library.ualberta.ca/files/c3j333244m.

Council of Science Editors:

James K. Deciphering the mechanism(s) which limit reovirus spread in resistant lung and HNSCC cancer cells. [Masters Thesis]. University of Alberta; 2016. Available from: https://era.library.ualberta.ca/files/c3j333244m

28. Green, Nicole Marie. Coordination of muscle maintenance and innate immunity through integrated tissue physiology in Drosphila.

Degree: PhD, Biochemistry and Molecular Biophysics Interdepartmental Program, 2018, Kansas State University

URL: http://hdl.handle.net/2097/39128

► Maintenance of muscle tissue during development is greatly dependent upon the extracellular matrix (ECM) to stabilize, sense, and compensate for changes in the local environment.… (more)

▼ Maintenance of muscle tissue during development is greatly dependent upon the extracellular matrix (ECM) to stabilize, sense, and compensate for changes in the local environment. Muscle has a particularly high demand for a dynamic ECM to allow for contraction and to transmit forces necessary for generating movement. Inefficient contraction and/or detachment can lead to muscle tissue damage and the release of damage-associated molecular patterns (DAMPs), which overactivate immune responses and drive the progression of muscle diseases. Our lab uses the Drosophila muscle attachment site (MAS) as a model to characterize novel genes and mechanisms involved in muscle maintenance. Initially, we were focused on characterizing a novel ECM protein, Fondue (Fon), which had previously been shown as a critical mediator of ECM stability in the hemolymph clot. Mutations in fon and the knockdown of fon through RNAi causes body wall muscles to detach and also creates large gaps between muscle hemisegments. TEM analysis of fon mutant MASs revealed a loss of ECM integrity and important support features including disruption of cuticle and tendon architectures, a lack of muscle-tendon interdigitation, and a loss of electron-dense matrix accumulation. More interestingly, a sensitized background screen revealed a subset of coagulation proteins, fon, Tiggrin, and Lsp1γ, that were necessary for stabilizing muscle attachment sites. Further investigation into gene expression profiles of mutants experiencing hypercontraction-induced muscle tissue stress indicated a clear trend of innate immune activation, suggesting a broader connection between muscle development and innate immunity. In fon mutants with muscle detachment, we also observe abnormal melanin accumulation as melanotic tumors or along the larval MASs, activation of Toll signaling in the fat body, and constitutive expression of the antimicrobial peptide (AMP), drosomycin. In a fon-sensitized background assay, we identified genetic interactions between fon and Toll pathway members, including the NFκB inhibitor/IκB, cactus. At the local level, fon-mediated muscle detachment and muscle hypercontraction mutants, Mhc[superscript]S1 and Brkd[superscript]J29, cause JAK/STAT activation within muscle tissue. We propose a model where muscle tissue stress caused by disruptions to muscle homeostasis progresses muscle disease through overactivation of the innate immune system. Understanding the mechanisms by which these two biological processes are intertwined will advance our knowledge of how tissue stresses can be sensed and elicit multi-tissue responses. Advisors/Committee Members: Erika R. Geisbrecht.

Subjects/Keywords: muscle; innate immunity; Drosophila; tissue maintenance

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Green, N. M. (2018). Coordination of muscle maintenance and innate immunity through integrated tissue physiology in Drosphila. (Doctoral Dissertation). Kansas State University. Retrieved from http://hdl.handle.net/2097/39128

Chicago Manual of Style (16^th Edition):

Green, Nicole Marie. “Coordination of muscle maintenance and innate immunity through integrated tissue physiology in Drosphila.” 2018. Doctoral Dissertation, Kansas State University. Accessed January 19, 2020. http://hdl.handle.net/2097/39128.

MLA Handbook (7^th Edition):

Green, Nicole Marie. “Coordination of muscle maintenance and innate immunity through integrated tissue physiology in Drosphila.” 2018. Web. 19 Jan 2020.

Vancouver:

Green NM. Coordination of muscle maintenance and innate immunity through integrated tissue physiology in Drosphila. [Internet] [Doctoral dissertation]. Kansas State University; 2018. [cited 2020 Jan 19]. Available from: http://hdl.handle.net/2097/39128.

Council of Science Editors:

Green NM. Coordination of muscle maintenance and innate immunity through integrated tissue physiology in Drosphila. [Doctoral Dissertation]. Kansas State University; 2018. Available from: http://hdl.handle.net/2097/39128

University of Newcastle

29. Hsu, Alan (Chen-Yu). Mechanism of infection of bronchial epithelial cells by human and avian influenza viruses.

Degree: PhD, 2010, University of Newcastle

URL: http://hdl.handle.net/1959.13/917312

►

Research Doctorate - Doctor of Philosophy (PhD)

Respiratory epithelial cells including bronchial epithelial cells (BECs) are the initial site of infection with influenza viruses, and… (more)

▼

Research Doctorate - Doctor of Philosophy (PhD)

Respiratory epithelial cells including bronchial epithelial cells (BECs) are the initial site of infection with influenza viruses, and the anti-viral responses elicited by these cells are a critical first line of defense against respiratory viral infection and can induce effective adaptive immune responses. However, relatively little is known about the importance of this innate anti-viral response, and the magnitude and effectiveness of this response is poorly understood. In addition to human influenza, avian influenza viruses are a potential source of future pandemics, therefore it is also critical to examine the effectiveness of the host anti-viral system to low and high pathogenic avian influenza viruses. Anti-viral responses to a human influenza H3N2, a low pathogenic avian influenza H11N9 and a high pathogenic avian influenza H5N1 was profiled using Calu-3 cells and primary bronchial epithelial cells (pBECs) to model proximal airway cells and A549 cells to reflect alveolar cells. The susceptibility of BECs to influenza infection was not solely dependent on the sialic acid-bearing glycoprotein expression and was affected by the apoptosis and anti-viral responses after infection. The earlier and greater anti-viral signaling and protein production correlated with the control of infection. However the H3N2 strain resulted in a delay in anti-viral signaling and impaired release of type I and type III interferons (IFNs) compared to the H11N9 virus. The differences in anti-viral induction between H3N2 and H11N9 were partly due to the influenza non-structural (NS) 1 protein. The gene encoding for NS1 was transfected into the BECs and the H3N2 NS1 induced a greater inhibition of anti-viral responses compared to the H11N9 NS1. Regardless of this inhibition by the influenza viruses, the constitutive secretion of IFN-β by BECs played a more critical role in inducing late anti-viral signaling via type I IFN receptors and was crucial in limiting viral infection by apoptosis. Infection with H5N1 resulted in a complete abolishment of this response in the infected BECs, including those induced by the constitutive IFN-β. This was due to the robust inhibition of host anti-viral responses by the NS1 protein of H5N1. This study characterizes anti-influenza virus responses in airway epithelial cells and shows for the first time that constitutive IFN-β release plays an important role in initiating protective late IFN-stimulated responses during influenza infection in airway epithelial cells. In addition, the subversion of human anti-viral responses may be an important requirement for influenza viruses to adapt to the human host and induce disease. Furthermore by understanding both of these avenues will identify targets for potential therapeutics.

Advisors/Committee Members: University of Newcastle. Faculty of Health, School of Medicine and Public Health.

Subjects/Keywords: influenza; innate immunity; bronchial epithelial cells

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Hsu, A. (. (2010). Mechanism of infection of bronchial epithelial cells by human and avian influenza viruses. (Doctoral Dissertation). University of Newcastle. Retrieved from http://hdl.handle.net/1959.13/917312

Chicago Manual of Style (16^th Edition):

Hsu, Alan (Chen-Yu). “Mechanism of infection of bronchial epithelial cells by human and avian influenza viruses.” 2010. Doctoral Dissertation, University of Newcastle. Accessed January 19, 2020. http://hdl.handle.net/1959.13/917312.

MLA Handbook (7^th Edition):

Hsu, Alan (Chen-Yu). “Mechanism of infection of bronchial epithelial cells by human and avian influenza viruses.” 2010. Web. 19 Jan 2020.

Vancouver:

Hsu A(. Mechanism of infection of bronchial epithelial cells by human and avian influenza viruses. [Internet] [Doctoral dissertation]. University of Newcastle; 2010. [cited 2020 Jan 19]. Available from: http://hdl.handle.net/1959.13/917312.

Council of Science Editors:

Hsu A(. Mechanism of infection of bronchial epithelial cells by human and avian influenza viruses. [Doctoral Dissertation]. University of Newcastle; 2010. Available from: http://hdl.handle.net/1959.13/917312

University of Newcastle

30. Tay, Hock Luck. The role of microRNA in regulating antibacterial responses in innate immune cells.

Degree: PhD, 2014, University of Newcastle

URL: http://hdl.handle.net/1959.13/1041634

►

Research Doctorate - Doctor of Philosophy (PhD)

Respiratory infections are one of the major burdens to public health due to the ease of transmission and… (more)

▼

Research Doctorate - Doctor of Philosophy (PhD)

Respiratory infections are one of the major burdens to public health due to the ease of transmission and affect people of all ages. Respiratory infections are common and normal host defence mechanisms in the lung and are often adequate in clearing the invading pathogen. Infections, however, can be persistent or life threatening if patients have an underlying lung diseases such as chronic obstructive pulmonary disease (COPD) or if they are immunocompromised. Understanding the mechanisms and pathways responsible for regulating the host defence response to lung infections is central to developing new and novel therapeutic strategies. While the role of molecules such as pattern recognition receptors (PRRs) and the downstream signalling events they initiate to activate host defence has been extensively studied, the post-transcriptional regulation of molecules that are involved in immune regulation are just beginning to be explored. MicroRNAs are small non-coding RNA that bind to multiple target mRNA and regulate gene expression post-transcriptionally by repressing protein production. The role of miRNAs in initiating and controlling inflammation through cytokine production and toll-like receptor regulation in response to pathogens has received much attention. However, the role of specific miRNAs during bacterial lung infection, pathogen killing and phagocytosis remain unknown. Using a well-characterised model of respiratory infection with non-typeable Haemophilus Influenzae (NTHi), we show that miRNA-328 (miR-328) is downregulated in the lungs during NTHi infection. Further studies showed that pharmacological inhibition of miR-328 in vitro increased phagocytosis of bacteria by macrophages and neutrophils. Similarly, inhibiting miR-328 during infection of the lung improved bacterial clearance under normal conditions, and during heightened susceptibility to infection promoted by immune-suppression, and smoking-induced emphysema. Our studies uncover a novel role for miRNA in the regulation of phagocytosis and indicate the potential for the inhibition of miR-328 as a therapy for antibiotic resistant bacterial infections in the lung.

Advisors/Committee Members: University of Newcastle. Faculty of Health & Medicine, School of Biomedical Sciences and Pharmacy.

Subjects/Keywords: microRNA; respiratory disease; microbial infection; innate immunity

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Tay, H. L. (2014). The role of microRNA in regulating antibacterial responses in innate immune cells. (Doctoral Dissertation). University of Newcastle. Retrieved from http://hdl.handle.net/1959.13/1041634

Chicago Manual of Style (16^th Edition):

Tay, Hock Luck. “The role of microRNA in regulating antibacterial responses in innate immune cells.” 2014. Doctoral Dissertation, University of Newcastle. Accessed January 19, 2020. http://hdl.handle.net/1959.13/1041634.

MLA Handbook (7^th Edition):

Tay, Hock Luck. “The role of microRNA in regulating antibacterial responses in innate immune cells.” 2014. Web. 19 Jan 2020.

Vancouver:

Tay HL. The role of microRNA in regulating antibacterial responses in innate immune cells. [Internet] [Doctoral dissertation]. University of Newcastle; 2014. [cited 2020 Jan 19]. Available from: http://hdl.handle.net/1959.13/1041634.

Council of Science Editors:

Tay HL. The role of microRNA in regulating antibacterial responses in innate immune cells. [Doctoral Dissertation]. University of Newcastle; 2014. Available from: http://hdl.handle.net/1959.13/1041634

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Open Access Theses and Dissertations