诱导共刺激分子（ICOS）对于实验性自身免疫性重症肌无力的发展至关重要。
ICOS is essential for the development of experimental autoimmune myasthenia gravis.
作者信息
Scott Benjamin G, Yang Huan, Tüzün Erdem, Dong Chen, Flavell Richard A, Christadoss Premkumar
机构信息
Department of Microbiology and Immunology, The University of Texas Medical Branch, 301 University Boulevard, 3.142 MRB, Galveston, TX 77555-1070, USA.
出版信息
J Neuroimmunol. 2004 Aug;153(1-2):16-25. doi: 10.1016/j.jneuroim.2004.04.019.
Lymphocyte costimulation via the inducible costimulatory molecule (ICOS) is required for effective humoral immunity development. Following immunization with Torpedo acetylcholine receptor (AChR), ICOS gene knockout (KO) mice were highly resistant to clinical experimental autoimmune myasthenia gravis (EAMG) development, had less serum AChR-specific immunoglobulins (Igs), and exhibited a diminutive germinal center (GC) reaction in secondary lymphoid tissues. Lymphocyte proliferation and both Th1 and Th2 differentiation in response to AChR and the AChR dominant alpha146-162 peptide were inhibited by the ICOS gene deficiency. ICOS-mediated lymphocyte costimulation is thus vital to the induction of T cell-mediated humoral immunity to AChR and the development of clinical EAMG.
通过诱导性共刺激分子（ICOS）进行的淋巴细胞共刺激是有效体液免疫发展所必需的。在用鱼雷乙酰胆碱受体（AChR）免疫后，ICOS基因敲除（KO）小鼠对临床实验性自身免疫性重症肌无力（EAMG）的发展具有高度抗性，血清中AChR特异性免疫球蛋白（Igs）较少，并且在二级淋巴组织中表现出微小的生发中心（GC）反应。ICOS基因缺陷抑制了淋巴细胞增殖以及对AChR和AChR显性α146 - 162肽的Th1和Th2分化。因此，ICOS介导的淋巴细胞共刺激对于诱导针对AChR的T细胞介导的体液免疫以及临床EAMG的发展至关重要。
Zotero 插件