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首页> 外文期刊>Autoimmunity reviews >Viral connection between drug rashes and autoimmune diseases: how autoimmune responses are generated after resolution of drug rashes.
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Viral connection between drug rashes and autoimmune diseases: how autoimmune responses are generated after resolution of drug rashes.

机译：皮疹与自身免疫性疾病之间的病毒联系：解决皮疹后如何产生自身免疫反应。

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摘要

Viral infections are most likely triggering factors of autoimmune diseases, although a single vial infection is not sufficient to cause clinically evident autoimmune diseases. Any disease that profoundly alters the immune system may cause perturbed viral infections, thereby rendering otherwise refractory patients susceptible to autoimmune diseases. In this regard, drug-induced hypersensitivity syndrome (DIHS), a drug rash characterized by sequential reactivations of herpesviruses and the subsequent development of autoimmune diseases, offers a unique opportunity to investigate the mechanism of how autoimmunity is elicited after viral infections. Indeed, several autoimmune diseases have been reported to occur at intervals of several months to years after clinical resolution of DIHS. Two representative cases who developed autoimmune diseases three to four years after DIHS are shown. Our recent analyses of the kinetics of a developing disease have shown that fully functional FoxP3(+) regulatory T (Treg) cells are expanded at the acute stage thereby allowing viral reactivations but lose their suppressive function coincident with their contraction upon clinical resolution. The functional defect of Treg cells would be responsible for the subsequent development of autoimmune diseases. Patients with DIHS need close monitoring because of possible progression to autoimmune diseases even after the complete resolution.
机译：病毒感染最有可能是自身免疫性疾病的触发因素，尽管单个小瓶感染不足以引起临床上明显的自身免疫性疾病。任何严重改变免疫系统的疾病都可能引起病毒感染，从而使难治性患者易患自身免疫性疾病。在这方面，药物诱发的超敏反应综合征（DIHS）是一种以皮疹病毒的顺序重新激活和随后的自身免疫疾病发展为特征的皮疹，为研究病毒感染后如何引发自身免疫的机制提供了独特的机会。实际上，已经报道了几种自身免疫性疾病，在DIHS临床解决后的数月至数年间发生。显示了在DIHS后三到四年发展为自身免疫性疾病的两个代表性病例。我们对正在发生的疾病的动力学的最新分析表明，功能全面的FoxP3（+）调节性T（Treg）细胞在急性期会扩增，从而允许病毒重新激活，但失去其抑制功能，并伴随其在临床上的收缩而收缩。 Treg细胞的功能缺陷将导致自身免疫疾病的后续发展。 DIHS患者需要密切监测，因为即使完全解决后也可能发展为自身免疫性疾病。

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