The analysis of development of autoimmune disease and abnormalexpansion of B-1 cells in G5PR transgenic mice

在自身免疫性疾病中，自身反应性B细胞被激活并产生自身抗体，导致组织损伤。我们发现丝氨酸/苏氨酸蛋白磷酸酶2A的B“调节亚基之一G5 PR的异常表达可诱导小鼠腹腔内B-1a细胞的扩增和自身抗体的产生。G5 PR在B-1a细胞中的过表达抑制了JNK介导的凋亡信号通路，并从抗原刺激激活诱导的细胞死亡中拯救出来。这些结果表明，G5 PR可能在B细胞选择B-1a细胞和自身免疫性疾病的发展中起关键作用。

In the autoimmune disease, auto-reactive B cells are activated and produce theautoantibodies, which induce the tissue injury. We found that abnormal expression of G5PR,one of the B’’ regulatory subunit of the serine/threonine protein phosphatase 2A,induced the expansion of B-1a cells in the peritoneal cavity and generation ofautoantibodies in mice. Over-expression of G5PR in B-1a cells suppressed the JNK-mediatedapoptotic signal pathway and rescued from activation-induced cell death by antigenstimulation. These results suggest that G5PR may play a pivotal role in B cell selectionfor B-1a cells and in the development of autoimmune disease.