In the past decades, clinical and experimental evidence has demonstrated that psoriasis is an immune‐mediated inflammatory disease of the skin that occurs in genetically susceptible individuals. Psoriasis also shows clear autoimmune pathomechanisms, but specific cellular targets for the onset and maintenance of psoriatic lesions were not established until 2014. Since then, four psoriasis autoantigens were discovered, namely cathelicidin LL‐37, melanocytic ADAMTSL5, lipid antigen PLA2G4D and keratin 17. Autoreactive T cells against these autoantigens were found in a number of patients with moderate‐to‐severe plaque psoriasis. Moreover, the discovery of autoantibodies against LL‐37 and ADAMTSL5 and their strong association with psoriatic arthritis (PsA) suggest a potential role of these autoantibodies in the pathogenesis of PsA. This review discusses the current studies on psoriatic autoantigens and the associated circulating autoantibodies and their mechanisms involved in the development and maintenance of psoriatic plaques. Recent autoimmune evidence fuelled the discussion on psoriasis as an autoimmune skin disorder and has the potential to develop new treatment strategies with protective and therapeutic antigen‐targeted methods.

中文翻译：

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银屑病中自身抗原和自身抗体的最新知识。

在过去的几十年中，临床和实验证据表明，牛皮癣是一种免疫介导的皮肤炎症性疾病，发生在遗传易感人群中。银屑病也显示出清晰的自身免疫机制，但直到2014年才确立了牛皮癣病变发作和维持的特异性细胞靶标。此后，发现了四种牛皮癣自身抗原，即cathelicidin LL-37，黑素细胞ADAMTSL5，脂质抗原PLA2G4D和角蛋白17。在许多中度至重度斑块状牛皮癣患者中发现了针对这些自身抗原的自身反应性T细胞。此外，针对LL-37和ADAMTSL5的自身抗体的发现以及它们与银屑病关节炎（PsA）的强相关性表明，这些自身抗体在PsA的发病机理中具有潜在的作用。这篇综述讨论了有关银屑病自身抗原和相关循环自身抗体及其机制参与银屑病斑块形成和维持的最新研究。最近的自身免疫证据激起了关于牛皮癣作为自身免疫性皮肤病的讨论，并有可能通过保护性和治疗性抗原靶向方法开发新的治疗策略。