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020 ▼a 9780438364943
035 ▼a (MiAaPQ)AAI10984435
040 ▼a MiAaPQ ▼c MiAaPQ ▼d 248032
0820 ▼a 616.079
1001 ▼a Zhang, Qianxia.
24510 ▼a Intrinsic Mechanisms Regulating T Cell Tolerance in Autoimmune Diabetes.
260 ▼a [S.l.] : ▼b University of Pittsburgh., ▼c 2018
260 1 ▼a Ann Arbor : ▼b ProQuest Dissertations & Theses, ▼c 2018
300 ▼a 171 p.
500 ▼a Source: Dissertation Abstracts International, Volume: 80-01(E), Section: B.
500 ▼a Adviser: Dario A. A. Vignali.
5021 ▼a Thesis (Ph.D.)--University of Pittsburgh, 2018.
520 ▼a 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
520 ▼a 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
520 ▼a 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
590 ▼a School code: 0178.
650 4 ▼a Immunology.
690 ▼a 0982
71020 ▼a University of Pittsburgh.
7730 ▼t Dissertation Abstracts International ▼g 80-01B(E).
773 ▼t Dissertation Abstract International
790 ▼a 0178
791 ▼a Ph.D.
792 ▼a 2018
793 ▼a English
85640 ▼u http://www.riss.kr/pdu/ddodLink.do?id=T15001403 ▼n KERIS
980 ▼a 201812 ▼f 2019
990 ▼a 관리자