Interleukin-33 alleviates psoriatic inflammation by suppressing the T helper type 17 immune response.,Immunology

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Interleukin-33 alleviates psoriatic inflammation by suppressing the T helper type 17 immune response.
Immunology ( IF 4.9 ) Pub Date : 2020-04-18 , DOI: 10.1111/imm.13203
Zeyu Chen _{1,

2} , Yifan Hu _{1,

2} , Yu Gong _{1,

2} , Xilin Zhang _{2,

3} , Lian Cui _{1,

2} , Rongfen Chen _{1,

2} , Yingyuan Yu _{1,

2} , Qian Yu _{1,

2} , Youdong Chen _{1,

2} , Hongyue Diao _{1,

2} , Jia Chen ₄ , Yuanyuan Wang _{1,

2} , Yuling Shi _{1,

2}

Affiliation

Psoriasis is a chronic inflammatory skin disease with unclear pathogenesis. Interleukin‐33 (IL‐33) is highly expressed in patients with psoriasis, but its role in psoriasis is unknown. The aim of this study was to investigate the possible role of IL‐33 in the pathogenesis and treatment of psoriasis. IL‐33 expression was determined using enzyme‐linked immunosorbent assay, real‐time fluorescent quantitative polymerase chain reaction and immunohistochemical staining. CD4⁺ T cells were sorted using magnetic beads and treated with or without IL‐33. Imiquimod (IMQ) was used to induce psoriatic inflammation in mice. The frequency of immune cells was determined using flow cytometry. The cytokine level in mouse skin was measured using cytometric bead array. Our results showed that IL‐33 was highly expressed in the lesional skin and serum of patients with moderate‐to‐severe plaque psoriasis. IL‐33 inhibited the expression of IL‐17 in CD4⁺ T cells of psoriasis patients. Subcutaneous injection of IL‐33 alleviated the IMQ‐induced psoriatic inflammation in mice, reduced tumor necrosis factor‐α and IL‐23 expression, and decreased the proportion of T helper type 17 (Th17) cells in the skin‐draining lymph nodes in the mice. Our results suggest that IL‐33 plays a protective role in the pathogenesis of psoriasis by suppressing Th17 cell differentiation and function. The potential therapeutic effect of IL‐33 in treating psoriasis warrants further investigation.

中文翻译：

Interleukin-33 通过抑制 T 辅助细胞 17 型免疫反应减轻银屑病炎症。

银屑病是一种发病机制不明的慢性炎症性皮肤病。白细胞介素-33（IL-33）在银屑病患者中高表达，但其在银屑病中的作用尚不清楚。本研究的目的是探讨 IL-33 在银屑病的发病机制和治疗中的可能作用。IL-33 表达使用酶联免疫吸附试验、实时荧光定量聚合酶链反应和免疫组织化学染色确定。CD4 ⁺使用磁珠分选 T 细胞，并用或不用 IL-33 处理。咪喹莫特 (IMQ) 用于诱导小鼠的银屑病炎症。使用流式细胞术测定免疫细胞的频率。使用细胞计数珠阵列测量小鼠皮肤中的细胞因子水平。我们的结果表明 IL-33 在中度至重度斑块状银屑病患者的皮损皮肤和血清中高表达。IL-33抑制银屑病患者CD4 ⁺ T细胞中IL-17的表达。皮下注射IL-33可减轻IMQ诱导的小鼠银屑病炎症，降低肿瘤坏死因子-α和 IL-23 表达，并降低小鼠皮肤引流淋巴结中 T 辅助 17 型 (Th17) 细胞的比例。我们的结果表明 IL-33 通过抑制 Th17 细胞分化和功能在银屑病的发病机制中发挥保护作用。IL-33 在治疗银屑病方面的潜在治疗效果值得进一步研究。

更新日期：2020-04-18

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