Psoriasis is an immune cell-dependent chronic autoimmune skin disorder. Interleukin 37 (IL-37) is a cytokine belonging to the IL-1 family that shows anti-inflammatory and protective effects in various mouse models of psoriasis. Even though various animal models are used to investigate the pathogenic mechanisms of psoriasis, human clinical studies are still needed to make up for the deficiencies, as animal models generally do not exhibit the complex phenotypic features of human psoriasis. Our study aims to demonstrate the relationship between IL-37-producing tissue-resident immune cells with the pathogenesis of psoriasis. The present study was performed on 28 psoriasis patients and 17 healthy volunteers. The ability of anti-inflammatory cytokine IL-37 to impede inflammation and regulate metabolic pathways was assessed by real-time quantitative polymerase chain reaction. Finally, immunofluorescence double staining for CD4⁺IL-37b⁺, CD68⁺IL-37b⁺, and (forkhead box protein P3) Foxp3⁺IL-37b⁺ was performed. The proportion of CD4⁺IL-37b⁺ T cells, CD68⁺IL-37b⁺ macrophages, and Foxp3⁺IL-37b⁺ T regulatory (Treg) cells was significantly increased in the psoriasis group compared to the control group. IL-37 gene expression was downregulated in psoriasis when contrasted to the control group. Our findings disclosed that IL-37-producing tissue-resident immune cells might be involved in the pathogenesis of psoriasis, and thus may be a therapeutic target for individuals with psoriasis.

中文翻译：

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银屑病病灶活检中 IL-37 基因表达降低，产生 IL-37 的组织驻留免疫细胞升高

牛皮癣是一种免疫细胞依赖性慢性自身免疫性皮肤病。白细胞介素 37 (IL-37) 是一种属于 IL-1 家族的细胞因子，在各种牛皮癣小鼠模型中显示出抗炎和保护作用。尽管多种动物模型被用来研究银屑病的发病机制，但仍需要人类临床研究来弥补缺陷，因为动物模型通常不表现出人类银屑病的复杂表型特征。我们的研究旨在证明产生 IL-37 的组织驻留免疫细胞与银屑病发病机制之间的关系。本研究针对 28 名银屑病患者和 17 名健康志愿者进行。通过实时定量聚合酶链反应评估抗炎细胞因子 IL-37 阻止炎症和调节代谢途径的能力。最后，进行CD4 ⁺ IL-37b ⁺、CD68 ⁺ IL-37b ⁺和（叉头盒蛋白P3）Foxp3 ⁺ IL-37b ^{+的免疫荧光双染色。}与对照组相比，银屑病组CD4 ⁺ IL-37b ⁺ T 细胞、CD68 ⁺ IL-37b ⁺巨噬细胞和 Foxp3 ⁺ IL-37b ⁺ T 调节性（Treg）细胞的比例显着增加。与对照组相比，银屑病中 IL-37 基因表达下调。我们的研究结果表明，产生 IL-37 的组织驻留免疫细胞可能参与银屑病的发病机制，因此可能是银屑病患者的治疗靶点。