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You searched for +publisher:"University of North Carolina" +contributor:("Sheikh, Shehzad"). Showing records 1 – 3 of 3 total matches.

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University of North Carolina

1. Hong, Lee. CD30-REDIRECTED CHIMERIC ANTIGEN RECEPTOR T CELLS TARGET EMBRYONAL CARCINOMA VIA ANTIGEN-DEPENDENT AND FAS/FASL INTERACTIONS.

Degree: Microbiology and Immunology, 2018, University of North Carolina

Embryonal carcinomas (ECs) and mixed testicular germ cell tumors (TGCTs) containing EC express CD30 and are the most aggressive TGCT subtypes. Chimeric antigen receptor T cells (CAR-Ts) combine the cytotoxic properties of T cells with the antigen specificity of monoclonal antibodies to target antigen-expressing cells, such as infected or cancerous cells. CAR-Ts targeting CD30 (CD30.CAR-Ts) have shown robust anti-tumor activity against Hodgkin’s lymphoma, but have not been tested against solid tumors. We tested whether CD30.CAR-Ts could also target ECs using in vitro and in vivo models. CD30.CAR-Ts exhibited anti-tumor activity in vitro against the human EC cell lines Tera-1, Tera-2 and NCCIT, and putative EC stem cells identified by Hoechst dye staining. Cytolytic activity of CD30.CAR-Ts was complemented by sustained proliferation and pro-inflammatory cytokine production. CD30.CAR-Ts also demonstrated anti-tumor activity in an in vivo xenograft NSG mouse model of metastatic EC. Remarkably, we observed that CD30.CAR-Ts, while targeting CD30+ EC tumor cells through the CAR (i.e. antigen-dependent targeting), also eliminated surrounding CD30– EC cells in an antigen-independent manner via cell-cell contact-dependent Fas/FasL interaction. In addition, inducing Fas (CD95) expression in CD30+ but Fas– EC was sufficient to improve CD30.CAR-T anti-tumor activity. Overall, these data suggest that CD30.CAR-Ts can be used as a novel immunotherapy for ECs. Additionally, Fas/FasL interaction between tumor cells and CAR-Ts can be exploited to reduce tumor escape due to heterogeneous antigen expression or to improve CAR-T anti-tumor activity. Advisors/Committee Members: Hong, Lee, Dotti, Gianpietro, Tisch, Roland, Savoldo, Barbara, Whitmire, Jason, Wan, Yisong, Sheikh, Shehzad.

Subjects/Keywords: School of Medicine; Department of Microbiology and Immunology

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

APA (6th Edition):

Hong, L. (2018). CD30-REDIRECTED CHIMERIC ANTIGEN RECEPTOR T CELLS TARGET EMBRYONAL CARCINOMA VIA ANTIGEN-DEPENDENT AND FAS/FASL INTERACTIONS. (Thesis). University of North Carolina. Retrieved from https://cdr.lib.unc.edu/record/uuid:519f1372-1638-487e-b82e-0681308db3e0

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):

Hong, Lee. “CD30-REDIRECTED CHIMERIC ANTIGEN RECEPTOR T CELLS TARGET EMBRYONAL CARCINOMA VIA ANTIGEN-DEPENDENT AND FAS/FASL INTERACTIONS.” 2018. Thesis, University of North Carolina. Accessed October 31, 2020. https://cdr.lib.unc.edu/record/uuid:519f1372-1638-487e-b82e-0681308db3e0.

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

MLA Handbook (7th Edition):

Hong, Lee. “CD30-REDIRECTED CHIMERIC ANTIGEN RECEPTOR T CELLS TARGET EMBRYONAL CARCINOMA VIA ANTIGEN-DEPENDENT AND FAS/FASL INTERACTIONS.” 2018. Web. 31 Oct 2020.

Vancouver:

Hong L. CD30-REDIRECTED CHIMERIC ANTIGEN RECEPTOR T CELLS TARGET EMBRYONAL CARCINOMA VIA ANTIGEN-DEPENDENT AND FAS/FASL INTERACTIONS. [Internet] [Thesis]. University of North Carolina; 2018. [cited 2020 Oct 31]. Available from: https://cdr.lib.unc.edu/record/uuid:519f1372-1638-487e-b82e-0681308db3e0.

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

Council of Science Editors:

Hong L. CD30-REDIRECTED CHIMERIC ANTIGEN RECEPTOR T CELLS TARGET EMBRYONAL CARCINOMA VIA ANTIGEN-DEPENDENT AND FAS/FASL INTERACTIONS. [Thesis]. University of North Carolina; 2018. Available from: https://cdr.lib.unc.edu/record/uuid:519f1372-1638-487e-b82e-0681308db3e0

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


University of North Carolina

2. Roche, Kyle. Intrinsic regulation of quiescence and radioresistance in intestinal stem cells.

Degree: Cell Biology and Physiology, 2016, University of North Carolina

The intestinal epithelium regenerates every 5-7 days, a process that is facilitated by a pool of intestinal stem cells. Over the past decade, it has become apparent that the intestinal stem cell pool is diverse, containing at least two populations. Active stem cells (aISCs) are moderately proliferative and contribute to homeostatic regeneration, while reserve stem cells (rISCs) are slowly proliferative and facilitate regeneration following damage-induced loss of the aISC population. The genetic mechanisms required for the production and maintenance of rISCs are unknown. Sox9 is a transcription factor that has been shown to maintain stem cell populations in various tissues. In the intestinal epithelium, Sox9 is expressed in a gradient that negatively correlates with proliferative capacity. Transit-amplifying progenitors express the lowest levels of Sox9, while aISCs express intermediate levels, and cells expressing the highest levels of Sox9 are consistent with slowly cycling rISCs. In this dissertation, I will address the role that Sox9 plays in maintaining rISC function within the intestinal epithelium. I find that Sox9 is not only necessary for the production of a quiescent rISCs, but that it is also uniformly necessary for maintaining radioresistance within the rISC pool. This work identifies Sox9 as a novel intrinsic regulator of the rISC state. Advisors/Committee Members: Roche, Kyle, Otey, Carol, Magness, Scott, Sheikh, Shehzad, Goy, Michael F., Henning, Susan.

Subjects/Keywords: School of Medicine; Department of Cell Biology and Physiology

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

APA (6th Edition):

Roche, K. (2016). Intrinsic regulation of quiescence and radioresistance in intestinal stem cells. (Thesis). University of North Carolina. Retrieved from https://cdr.lib.unc.edu/record/uuid:91534062-64fa-4881-9c13-92b57864f0e7

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):

Roche, Kyle. “Intrinsic regulation of quiescence and radioresistance in intestinal stem cells.” 2016. Thesis, University of North Carolina. Accessed October 31, 2020. https://cdr.lib.unc.edu/record/uuid:91534062-64fa-4881-9c13-92b57864f0e7.

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

MLA Handbook (7th Edition):

Roche, Kyle. “Intrinsic regulation of quiescence and radioresistance in intestinal stem cells.” 2016. Web. 31 Oct 2020.

Vancouver:

Roche K. Intrinsic regulation of quiescence and radioresistance in intestinal stem cells. [Internet] [Thesis]. University of North Carolina; 2016. [cited 2020 Oct 31]. Available from: https://cdr.lib.unc.edu/record/uuid:91534062-64fa-4881-9c13-92b57864f0e7.

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

Council of Science Editors:

Roche K. Intrinsic regulation of quiescence and radioresistance in intestinal stem cells. [Thesis]. University of North Carolina; 2016. Available from: https://cdr.lib.unc.edu/record/uuid:91534062-64fa-4881-9c13-92b57864f0e7

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


University of North Carolina

3. Sheikh, Shehzad Zafar. Defects in Macrophage Specific Homeostatic Pathways in the Inflammatory Bowel Diseases.

Degree: Microbiology and Immunology, 2010, University of North Carolina

Intestinal macrophages are specialized to carry out their functions in the local antigen- and microbiota-rich environment. They are refractory to the induction of proinflammatory cytokines, yet still display potent phagocytic and bactericidal activity. These adaptations allow the intestinal macrophage to eradicate microbes that breach the intestinal epithelial barrier while maintaining local tissue homeostasis. The inflammatory bowel diseases, Crohn’s disease and ulcerative colitis, results from an inappropriately directed inflammatory response to the enteric microbiota in a genetically susceptible host. In contrast to the characteristic anti-inflammatory phenotypic and functional profile of normal intestinal macrophages, these macrophages react to luminal microbes and become potent producers of proinflammatory cytokines such as IL-12 family members. IL-12 and 23 are heterodimeric cytokines produced by macrophages and dendritic cells that are important bridges between innate and adaptive immunity. Although the molecular events that lead to the expression of IL-12 and Il-23 in macrophages through TLR signaling have been well defined, anti-inflammatory pathways that lead to inhibition of these cytokines in macrophages have not been fully elucidated. We identify two important homeostatic pathways; IFN-γ and HO-1 that regulate enteric microbiota-induced production of IL-12 and 23 by macrophages. IFN-γ inhibits TLR induced IL-23 expression in macrophages, and these events prevent the initiation and progression of spontaneous IL-23-driven experimental colitis in IL-10 deficient (IL-10-/-) mice. Moreover, we demonstrate that enteric microbiota-induced heme-oxygenase 1 (HO- 1) is critical in the prevention of experimental colitis, through inhibition of IL-12 family members and augmentation of macrophage microbicidal pathways. In our first study we demonstrate that IFN-γ has anti-inflammatory properties in murine models of Th1/Th17 mediated experimental colitis through attenuation of TLRmediated IL-23 expression in macrophages. In the second series of experiments, using germ-free WT and colitis-prone IL-10-/- mice we show that intestinal HO-1 expression induced by the enteric microbiota is an important homeostatic pathway. We also identify signaling pathways (MyDD88, MAPK and Pi3K) essential for HO-1 induction in macrophages. Finally, in our third study, protective effects of the HO-1 pathway were determined in Th2-mediated chronic colonic inflammation in T cell receptor- alpha (TCRα) deficient (-/-) mice. TCRα-/- mice exposed to carbon monoxide (CO) or treated with a pharmacologic HO-1 inducer demonstrated significant amelioration of active colitis. We demonstrate that HO-1 regulates mucosal innate immune responses in the TCRα-/- mouse through IL-10 induction in colonic macrophages. Advisors/Committee Members: Sheikh, Shehzad Zafar, Plevy, Scott E., University of North Carolina at Chapel Hill.

Subjects/Keywords: School of Medicine; Department of Microbiology and Immunology

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

APA (6th Edition):

Sheikh, S. Z. (2010). Defects in Macrophage Specific Homeostatic Pathways in the Inflammatory Bowel Diseases. (Thesis). University of North Carolina. Retrieved from https://cdr.lib.unc.edu/record/uuid:e9f3f872-ae20-4d52-b298-16b98164daa8

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):

Sheikh, Shehzad Zafar. “Defects in Macrophage Specific Homeostatic Pathways in the Inflammatory Bowel Diseases.” 2010. Thesis, University of North Carolina. Accessed October 31, 2020. https://cdr.lib.unc.edu/record/uuid:e9f3f872-ae20-4d52-b298-16b98164daa8.

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

MLA Handbook (7th Edition):

Sheikh, Shehzad Zafar. “Defects in Macrophage Specific Homeostatic Pathways in the Inflammatory Bowel Diseases.” 2010. Web. 31 Oct 2020.

Vancouver:

Sheikh SZ. Defects in Macrophage Specific Homeostatic Pathways in the Inflammatory Bowel Diseases. [Internet] [Thesis]. University of North Carolina; 2010. [cited 2020 Oct 31]. Available from: https://cdr.lib.unc.edu/record/uuid:e9f3f872-ae20-4d52-b298-16b98164daa8.

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

Council of Science Editors:

Sheikh SZ. Defects in Macrophage Specific Homeostatic Pathways in the Inflammatory Bowel Diseases. [Thesis]. University of North Carolina; 2010. Available from: https://cdr.lib.unc.edu/record/uuid:e9f3f872-ae20-4d52-b298-16b98164daa8

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

.