Decreased microRNA‐126 expression in psoriatic CD4+ T cells promotes T‐helper 17 cell differentiation and the formation of dermatitis in imiquimod‐induced psoriasis‐like mice. Issue 4 (21st December 2021)

• Record Type: Journal Article
• Authors: Wu, Ruifang; Li, Xin; Li, Siying; Tang, Guishao; Zhang, Suhan; Zhu, Yanshan; Zhang, Xiaochao; Deng, Min; Tan, Siqi; Luo, Shuangyan; Zhang, Qing; Zhao, Ming; Zhang, Peng; Su, Yuwen
• Is Part Of: Journal of dermatology. Volume 49:Issue 4(2022)
• Page Start: 432
• Page End: 440
• Publication Date: 2021-12-21
• Subjects: CD4+ T cells -- differentiation -- microRNA‐126 -- psoriasis -- T‐helper 17 cells; Dermatology -- Periodicals; Dermatology -- Japan -- Periodicals; Skin -- Diseases -- Periodicals; 616.5005
• DOI: 10.1111/1346-8138.16272
• Languages: English
• ISSNs: 0385-2407

Abstract

Abstract: Psoriasis is a chronic inflammatory skin disease with multiple genetic backgrounds, whose etiology and pathogenesis are still unclear. Complex T‐cell immune imbalance has been demonstrated to play an important role in pathogenesis of psoriasis. This study reported that microRNA‐126 (miR‐126) expression was decreased in CD4 + T cells of both psoriasis patients and psoriasis‐like mouse models and its expression was negatively correlated with the Psoriasis Area and Severity Index (PASI) score of psoriasis patients. Conditional Mir126 knockout in mouse CD4 + T cells can obviously aggravate the psoriasis‐like dermatitis and promote T‐helper (Th)1 and Th17 cells' infiltration in spleen of imiquimod (IMQ)‐induced psoriasis‐like mouse model. In addition, the mRNA expression of Il17a and Il17f were significantly increased in mouse naïve CD4 + T cells with Mir126 knockout after stimulating with CD3 and CD28. Compared with naïve CD4 + T cells, the expression of Mir126 was decreased in Th17 cells, and Mir126 knockout notably promoted the differentiation of naïve CD4 + T cells to Th17 cells as well as the mRNA expression of Il17a, Il17f, Rorc, and Il23R . Our results revealed that decreased miR‐126 in psoriatic CD4 + T cells might accelerate the formation of skin lesions through promoting the differentiation of Th17 cells, thus suggesting a potential intervention target for psoriasis.