Inhibitory IgG receptor FcγRIIB fails to inhibit experimental autoimmune myasthenia gravis pathogenesis
- 作者：Jing Li ; Erdem Tü ; zü ; n ; Xiong Rong Wu ; Hui Bin Qi ; Windy Allman ; Shamsher S. Saini ; Premkumar Christadoss
- 关键词：Myasthenia gravis ; Fcγ ; RIIB ; IL-6 ; IL-10 ; Autoimmunity
- 刊名：Journal of Neuroimmunology
- 出版年：2008
- 期刊代码：32_01655728
- 类别：neu
- 出版时间：February 2008
- 卷：194
- 期：1-2
- 页码：44-53
- 文件大小：975 K
摘要
Deficiency of the inhibitory FcγRIIB renders mice susceptible to autoimmune disorders characterized with cellular infiltration of target tissue. To analyze the role of FcγRIIB in an antibody-mediated autoimmune disease, experimental autoimmune myasthenia gravis (EAMG), FcγRIIB knockout (KO) and wild-type mice were immunized with acetylcholine receptor (AChR). In contrast with previous reports, FcγRIIB 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 FcγRIIB promotes antibody-mediated autoimmunity.