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You searched for +publisher:"University of North Carolina" +contributor:("Markovic-Plese, Silva"). Showing records 1 – 2 of 2 total matches.

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University of North Carolina

1. Blauth, Kevin. Fractalkine Induces the Expression of Intercellular Adhesion Molecule-1 on CD4+ T-lymphocytes: implications for the immunopathogenesis of Multiple Sclerosis.

Degree: 2012, University of North Carolina

Fractalkine (CX3CL1) is a chemokine that has been shown to play roles in lymphocyte chemotaxis, inflammation, and neuroprotection in central nervous system (CNS) diseases. Here we examined roles for CX3CL1 in CD4+ T-cell chemotaxis mediated via their upregulation of adhesion molecule expression as well as secretion of inflammatory cytokines involved in the pathogenesis of relapsing remitting multiple sclerosis (RRMS). We found that CX3CL1 concentrations are elevated in the cerebrospinal fluid (CSF) of RRMS patients, and that CX3CL1 increases mRNA expression of IFN-γ and TNF-α, and protein secretion of IFN-γ by CD4+ T-cells derived from RRMS patients but not those derived from healthy controls (HCs). We also show that blood-derived CD4+T-cells express increased surface levels of CX3CL1 receptor (CX3CR1) and intercellular adhesion molecule (ICAM)-1 in RRMS patients in comparison to HCs. Furthermore, the percentage of CX3CR1+ICAM-1+CD4+ T-cells are increased in the CSF of untreated RRMS patients in comparison to their peripheral blood samples, and CD4+ T-cells which migrate in-vitro toward a CX3CL1 gradient express higher levels of ICAM-1 than CD4+ T-cells that do not migrate. Furthermore, we demonstrated that CX3CL1 upregulates ICAM-1 expression on the surface of RRMS patient-derived but not HC derived CD4+ T-cells. Lastly, we show that CX3CL1 stimulates ICAM-1 expression on myelin-antigen-specific CD4+ T-cell lines derived from RRMS and healthy donors. These results indicate that CX3CL1 may preferentially recruit CX3CR1+ICAM-1+CD4+ T-cells into the CNS during RRMS development, and may activate CD4+ T-cells to express higher levels of ICAM-1, as well as the proinflammatory cytokines IFN-γ and TNF-α. Advisors/Committee Members: Blauth, Kevin, Markovic-Plese, Silva.

Subjects/Keywords: School of Medicine; UNC Neuroscience Center; Neuroscience Curriculum

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

APA (6th Edition):

Blauth, K. (2012). Fractalkine Induces the Expression of Intercellular Adhesion Molecule-1 on CD4+ T-lymphocytes: implications for the immunopathogenesis of Multiple Sclerosis. (Thesis). University of North Carolina. Retrieved from https://cdr.lib.unc.edu/record/uuid:2ceecd47-28bb-4eb7-93bb-c8b49fb10640

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

Chicago Manual of Style (16th Edition):

Blauth, Kevin. “Fractalkine Induces the Expression of Intercellular Adhesion Molecule-1 on CD4+ T-lymphocytes: implications for the immunopathogenesis of Multiple Sclerosis.” 2012. Thesis, University of North Carolina. Accessed October 31, 2020. https://cdr.lib.unc.edu/record/uuid:2ceecd47-28bb-4eb7-93bb-c8b49fb10640.

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

MLA Handbook (7th Edition):

Blauth, Kevin. “Fractalkine Induces the Expression of Intercellular Adhesion Molecule-1 on CD4+ T-lymphocytes: implications for the immunopathogenesis of Multiple Sclerosis.” 2012. Web. 31 Oct 2020.

Vancouver:

Blauth K. Fractalkine Induces the Expression of Intercellular Adhesion Molecule-1 on CD4+ T-lymphocytes: implications for the immunopathogenesis of Multiple Sclerosis. [Internet] [Thesis]. University of North Carolina; 2012. [cited 2020 Oct 31]. Available from: https://cdr.lib.unc.edu/record/uuid:2ceecd47-28bb-4eb7-93bb-c8b49fb10640.

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

Council of Science Editors:

Blauth K. Fractalkine Induces the Expression of Intercellular Adhesion Molecule-1 on CD4+ T-lymphocytes: implications for the immunopathogenesis of Multiple Sclerosis. [Thesis]. University of North Carolina; 2012. Available from: https://cdr.lib.unc.edu/record/uuid:2ceecd47-28bb-4eb7-93bb-c8b49fb10640

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


University of North Carolina

2. Freeman, Leslie. A Role for the NLR Family Members NLRC4 And NLRP3 in Astrocytic Inflammasome Activation and Astrogliosis.

Degree: 2016, University of North Carolina

The inflammasome is implicated in many inflammatory diseases but has been primarily studied in the macrophage-myeloid lineage. Here we demonstrate a physiologic role for nucleotide-binding domain, leucine-rich repeat, CARD domain containing 4 (NLRC4) in brain astrocytes. NLRC4 has been primarily studied in the context of gram-negative bacteria, where it is required for the maturation of pro-caspase-1 to active caspase-1. We show the heightened expression of NLRC4 protein in astrocytes in a cuprizone model of neuroinflammation and demyelination as well as human multiple sclerotic brains. Similar to macrophages, NLRC4 in astrocytes is required for inflammasome activation by its known agonist, flagellin. However, NLRC4 in astrocytes also mediate inflammasome activation in response to lysophosphatidylcholine (LPC), an inflammatory molecule associated with neurologic disorders. In addition to NLRC4, astrocytic NLRP3 is required for inflammasome activation by LPC. Two biochemical assays show the interaction of NLRC4 with NLRP3, suggesting the possibility of a NLRC4-NLRP3 co-inflammasome. Advisors/Committee Members: Freeman, Leslie, Ting, Jenny P.-Y., Matsushima, Glenn, Koller, Beverly H., Markovic-Plese, Silva, Kay Lund, Pauline Kay.

Subjects/Keywords: School of Medicine; Curriculum in Genetics and Molecular Biology

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

APA (6th Edition):

Freeman, L. (2016). A Role for the NLR Family Members NLRC4 And NLRP3 in Astrocytic Inflammasome Activation and Astrogliosis. (Thesis). University of North Carolina. Retrieved from https://cdr.lib.unc.edu/record/uuid:ec028a13-7c5a-41ed-af8d-3b5a5865278d

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

Chicago Manual of Style (16th Edition):

Freeman, Leslie. “A Role for the NLR Family Members NLRC4 And NLRP3 in Astrocytic Inflammasome Activation and Astrogliosis.” 2016. Thesis, University of North Carolina. Accessed October 31, 2020. https://cdr.lib.unc.edu/record/uuid:ec028a13-7c5a-41ed-af8d-3b5a5865278d.

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

MLA Handbook (7th Edition):

Freeman, Leslie. “A Role for the NLR Family Members NLRC4 And NLRP3 in Astrocytic Inflammasome Activation and Astrogliosis.” 2016. Web. 31 Oct 2020.

Vancouver:

Freeman L. A Role for the NLR Family Members NLRC4 And NLRP3 in Astrocytic Inflammasome Activation and Astrogliosis. [Internet] [Thesis]. University of North Carolina; 2016. [cited 2020 Oct 31]. Available from: https://cdr.lib.unc.edu/record/uuid:ec028a13-7c5a-41ed-af8d-3b5a5865278d.

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

Council of Science Editors:

Freeman L. A Role for the NLR Family Members NLRC4 And NLRP3 in Astrocytic Inflammasome Activation and Astrogliosis. [Thesis]. University of North Carolina; 2016. Available from: https://cdr.lib.unc.edu/record/uuid:ec028a13-7c5a-41ed-af8d-3b5a5865278d

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

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