自身免疫性疾病中FcgammaRs的激活和抑制

Springer seminars in immunopathology Pub Date : 2006-12-01 Epub Date: 2006-10-01 DOI:10.1007/s00281-006-0052-1
Falk Nimmerjahn
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引用次数: 58

摘要

自身免疫性疾病的特点是免疫系统破坏自身组织。在正常情况下,有多个检查点来防止自动反应。激活和抑制Fc受体(FcR)的共表达通过建立免疫细胞激活的阈值代表了这样一个检查点。然而,在许多人类自身免疫性疾病中,平衡的FcR表达受到干扰。对小鼠模型系统的分析提供了强有力的证据,表明异常的FcR表达可导致不受控制的免疫反应和自身免疫性疾病的启动。这篇综述将总结这些数据,并解释如何利用这些信息来更好地理解人类自身免疫性疾病和开发新的治疗策略。
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Activating and inhibitory FcgammaRs in autoimmune disorders.

Autoimmune disorders are characterized by the destruction of self-tissues by the immune system. Multiple checkpoints are in place to prevent autoreactivity under normal circumstances. Coexpression of activating and inhibitory Fc receptors (FcR) represents such a checkpoint by establishing a threshold for immune cell activation. In many human autoimmune diseases, however, balanced FcR expression is disturbed. Analysis of murine model systems provides strong evidence that aberrant FcR expression can result in uncontrolled immune responses and the initiation of autoimmune disease. This review will summarize this data and explain how this information might be used to better understand human autoimmune diseases and to develop novel therapeutic strategies.

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