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The m 6 A modification of Il17a in CD4 + T cells promotes inflammation in psoriasis.

Liyan YuanShijun ChenKe DingXiaobo WangWeiqi LvYuchen LiuShuang HeYingDian YuBin YangTao Huang
Published in: Experimental dermatology (2023)
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.
Keyphrases
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  • mouse model
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  • soft tissue