遗传变异、Fcγ 受体、KIR 与感染：自身免疫的进化。

Genetic variation, Fcγ receptors, KIRs and infection: the evolution of autoimmunity.

机构信息

Cambridge Institute for Medical Research, University of Cambridge School of Clinical Medicine, Box 139 Addenbrooke's Hospital, Hills Road, Cambridge CB2 0XY, UK.

出版信息

Curr Opin Immunol. 2010 Dec;22(6):715-22. doi: 10.1016/j.coi.2010.10.003. Epub 2010 Nov 1.

DOI:10.1016/j.coi.2010.10.003

PMID:21050737

Abstract

Recent work has emphasised the marked genetic variability that exists in the Fc receptor locus. This variation can contribute to the risk of autoimmune disease in both mice and humans, but can also have a profound impact on defence against infection. Using FcγRIIB and FcγRIIIB as examples, we demonstrate that variations associated with increased susceptibility to autoimmunity may be maintained in populations for their beneficial effect against infection. We examine the KIR locus from the same perspective and highlight similarities between the two loci. Intense selection pressure by pathogens presumably accounts for the marked variability within both regions and leads to susceptibility to autoimmunity for some alleles.

摘要

最近的研究强调了 Fc 受体基因座中存在的显著遗传多态性。这种变异既可以导致小鼠和人类自身免疫性疾病的发生风险，也可以对抗感染产生深远的影响。我们以 FcγRIIB 和 FcγRIIIB 为例，证明了与自身免疫易感性增加相关的变异可能在人群中得以保留，因为它们对感染具有有益的作用。我们从相同的角度研究了 KIR 基因座，并强调了这两个基因座之间的相似性。病原体的强烈选择压力可能导致这两个区域的显著变异性，并导致某些等位基因易患自身免疫性疾病。