抑制性免疫球蛋白G受体FcγRIIB无法抑制实验性自身免疫性重症肌无力的发病机制。

Inhibitory IgG receptor FcgammaRIIB fails to inhibit experimental autoimmune myasthenia gravis pathogenesis.

作者信息

Li Jing, Tüzün Erdem, Wu Xiong Rong, Qi Hui Bin, Allman Windy, Saini Shamsher S, Christadoss Premkumar

机构信息

Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX, 77555-1070, USA.

出版信息

J Neuroimmunol. 2008 Feb;194(1-2):44-53. doi: 10.1016/j.jneuroim.2007.11.005. Epub 2008 Jan 18.

DOI:10.1016/j.jneuroim.2007.11.005

PMID:18207575

Abstract

Deficiency of the inhibitory FcgammaRIIB renders mice susceptible to autoimmune disorders characterized with cellular infiltration of target tissue. To analyze the role of FcgammaRIIB in an antibody-mediated autoimmune disease, experimental autoimmune myasthenia gravis (EAMG), FcgammaRIIB knockout (KO) and wild-type mice were immunized with acetylcholine receptor (AChR). In contrast with previous reports, FcgammaRIIB KO mice were mildly resistant to EAMG despite preserved anti-AChR antibody production and neuromuscular junction complement deposition capacity. EAMG resistance was associated with reduced lymph node cell IL-6 and IL-10 production and increased CD4(+)CD25(+) cell ratios in lymph nodes. Our data suggest that FcgammaRIIB promotes antibody-mediated autoimmunity.

摘要

抑制性FcγRIIB的缺乏使小鼠易患以靶组织细胞浸润为特征的自身免疫性疾病。为了分析FcγRIIB在抗体介导的自身免疫性疾病——实验性自身免疫性重症肌无力（EAMG）中的作用，用乙酰胆碱受体（AChR）对FcγRIIB基因敲除（KO）小鼠和野生型小鼠进行免疫。与之前的报道相反，尽管FcγRIIB基因敲除小鼠保留了抗AChR抗体产生和神经肌肉接头补体沉积能力，但它们对EAMG有轻度抗性。EAMG抗性与淋巴结细胞IL-6和IL-10产生减少以及淋巴结中CD4(+)CD25(+)细胞比例增加有关。我们的数据表明，FcγRIIB促进抗体介导的自身免疫。