| First Author | Wu R | Year | 2022 |
| Journal | J Dermatol | Volume | 49 |
| Issue | 4 | Pages | 432-440 |
| PubMed ID | 34931339 | Mgi Jnum | J:355195 |
| Mgi Id | MGI:7737843 | Doi | 10.1111/1346-8138.16272 |
| Citation | Wu R, et al. (2022) 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. J Dermatol 49(4):432-440 |
| abstractText | 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 naive CD4(+) T cells with Mir126 knockout after stimulating with CD3 and CD28. Compared with naive CD4(+) T cells, the expression of Mir126 was decreased in Th17 cells, and Mir126 knockout notably promoted the differentiation of naive 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. |
