Psoriasis is a chronic inflammatory skin disease that involves numerous types of immune cells and cytokines resulting in an inflammatory feedback loop and hyperproliferation of the epidermis. A more detailed understanding of the underlying pathophysiology has revolutionized anti-psoriatic treatment and led to the development of various new drugs targeting key inflammatory cytokines such as IL-17A and IL-23. Successfully treated psoriatic lesions often resolve completely, leaving nothing visible to the naked eye. However, such lesions tend to recur within months at the exact same body sites. What is left behind at the cellular and molecular levels that potentially reinitiates psoriasis? Here, we elucidate the cellular and molecular “scar” and its imprints left after clinical resolution of psoriasis treated with anti-TNFα, anti-IL-17, or anti-IL-23 antibodies or phototherapy. Hidden cytokine stores and remaining tissue-resident memory T cells (TRMs) might hold the clue for disease recurrence.

中文翻译：

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斑块型牛皮癣的消退：留下的东西（并重新引发疾病）。

牛皮癣是一种慢性炎症性皮肤病，涉及多种类型的免疫细胞和细胞因子，导致炎症性反馈回路和表皮过度增殖。对潜在病理生理学的更详细了解已经彻底改变了抗银屑病的治疗方法，并导致开发出了针对关键炎症细胞因子（例如IL-17A和IL-23）的各种新药。成功治疗的牛皮癣病变通常会完全消退，肉眼看不见任何东西。但是，此类病变往往会在几个月内在完全相同的身体部位复发。在可能重新引发牛皮癣的细胞和分子水平上还剩下什么？在这里，我们将阐明在用抗TNFα，抗IL-17，抗肿瘤药物治疗牛皮癣的临床方法解决牛皮癣后留下的细胞和分子“疤痕”及其印记 或抗IL-23抗体或光疗。隐藏的细胞因子存储和剩余的组织驻留记忆T细胞（TRM）可能为疾病复发提供了线索。