Broegelmann Research Laboratory, Department of Clinical Science, University of Bergen, Bergen, Norway.
Vrije Universiteit Amsterdam, Amsterdam, The Netherlands.
Scand J Immunol. 2020 Oct;92(4):e12945. doi: 10.1111/sji.12945.
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.
在过去的几十年中，临床和实验证据表明，银屑病是一种发生在遗传易感个体中的皮肤免疫介导性炎症性疾病。银屑病也表现出明确的自身免疫病理机制，但直到 2014 年才确定了导致银屑病病变发生和维持的特定细胞靶点。此后，发现了四种银屑病自身抗原，即抗菌肽 LL-37、黑素细胞 ADAMTSL5、脂质抗原 PLA2G4D 和角蛋白 17。在许多中重度斑块型银屑病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，发现针对 LL-37 和 ADAMTSL5 的自身抗体及其与银屑病关节炎（PsA）的强烈关联表明这些自身抗体在 PsA 的发病机制中具有潜在作用。这篇综述讨论了银屑病自身抗原的当前研究以及相关的循环自身抗体及其在银屑病斑块发生和维持中的参与机制。最近的自身免疫证据推动了关于银屑病作为一种自身免疫性皮肤疾病的讨论，并有可能开发出具有保护和治疗性抗原靶向方法的新治疗策略。
