자료유형 | 학위논문 |
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서명/저자사항 | Intrinsic Mechanisms Regulating T Cell Tolerance in Autoimmune Diabetes. |
개인저자 | Zhang, Qianxia. |
단체저자명 | University of Pittsburgh. |
발행사항 | [S.l.]: University of Pittsburgh., 2018. |
발행사항 | Ann Arbor: ProQuest Dissertations & Theses, 2018. |
형태사항 | 171 p. |
기본자료 저록 | Dissertation Abstracts International 80-01B(E). Dissertation Abstract International |
ISBN | 9780438364943 |
학위논문주기 | Thesis (Ph.D.)--University of Pittsburgh, 2018. |
일반주기 |
Source: Dissertation Abstracts International, Volume: 80-01(E), Section: B.
Adviser: Dario A. A. Vignali. |
요약 | Type 1 Diabetes (T1D) is a polygenic autoimmune disease characterized by immune cell infiltration into the islets of Langerhans, destruction of insulin-producing beta cells, and uncontrolled hyperglycemia. Islet-antigen reactive CD4+ and CD8+ T |
요약 | Lymphocyte Activation Gene 3 (LAG3, CD223), a co-inhibitory receptor highly expressed on T cells, is one of these essential mechanisms that intrinsically regulate T cell tolerance in autoimmune diabetes. I evaluate the role of LAG3 on T cells ve |
요약 | In addition to dissecting the role of LAG3 in regulating T cell tolerance, I also show that removal of programmed death protein 1 (PD1) or overexpression of Neuropilin 1 (Nrp1) on Tregs protect NOD mice from autoimmune diabetes in Appendix A and |
일반주제명 | Immunology. |
언어 | 영어 |
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: 이 자료의 원문은 한국교육학술정보원에서 제공합니다. |