Mechanisms of Environment-Induced Autoimmunity.
Mechanisms of Environment-Induced Autoimmunity.
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DOI：
10.1146/annurev-pharmtox-031320-111453
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发表时间：
2021-01-06
影响因子：
12.5
通讯作者：
Kono DH
中科院分区：
文献类型：
--
作者：
Pollard KM;Cauvi DM;Mayeux JM;Toomey CB;Peiss AK;Hultman P;Kono DH
虽然许多环境暴露被认为是临床前自身免疫的触发因素，但只有少数环境暴露与自身免疫性疾病有自信的联系。对于与疾病相关的暴露，肺部是慢性暴露导致细胞毒性、组织损伤、炎症和纤维化的常见部位。暴露于颗粒物质会加剧这些特征，颗粒物质会阻碍清除和降解，从而促进持续的炎症。与暴露和由此产生的病理过程相一致的是自身抗原的翻译后修饰，这与含有丰富B细胞的三级淋巴样结构的形成相一致，被认为促进了自身抗体的产生，在某些情况下表现出主要的组织相容性复合物限制。在适当的基因-环境相互作用下，这些反应具有诊断特异性。更深入地了解控制这一过程的分子和细胞需求，特别是那些区分临床前自身免疫和临床自身免疫性疾病的分子和细胞需求，可能有助于确定环境暴露在人类自身免疫性疾病中的重要性。
Although numerous environmental exposures have been suggested as triggers for pre-clinical autoimmunity, only a few have been confidently linked to autoimmune diseases. For disease associated exposures, the lung is a common site where chronic exposure results in cellular toxicity, tissue damage, inflammation, and fibrosis. These features are exacerbated by exposures to particulate material, which hampers clearance and degradation thus facilitating persistent inflammation. Coincident with exposure and resulting pathological processes is the post-translational modification of self-antigens, which, in concert with the formation of tertiary lymphoid structures containing abundant B cells, is thought to promote the generation of autoantibodies that in some instances demonstrate major histocompatibility complex restriction. Under appropriate gene-environment interactions these responses can have diagnostic specificity. Greater insight into the molecular and cellular requirements governing this process, especially those that distinguish pre-clinical autoimmunity from clinical autoimmune disease, may facilitate determination of the significance of environmental exposures in human autoimmune disease.
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