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Psoriasis is a chronic inflammatory skin disorder. The mechanism of psoriasis pathogenesis is not entirely clear. Here, we reported that the level of the N6‐methyladenosine (m 6 A) modification was increased in psoriatic CD4 + T cells compared with healthy controls. In the psoriasis mouse model, depletion of the RNA demethylase, Alkbh5, from CD4 + T cells promoted the psoriasis‐like phenotype and inflammation. Intriguingly, this phenotype and inflammation were alleviated by the ablation of the m 6 A methyltransferase Mettl3 in CD4 + T cells. Mechanistically, we found that the m 6 A modification of IL17A mRNA increased the expression of IL‐17A (an important pro‐inflammatory factor in psoriasis) and promoted psoriasis. Thus, our study provided evidence that the m 6 A modification of IL17A in CD4 + T cells regulates inflammation in psoriasis.
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Yuan et al. (2023) studied this question.
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