蛋白质精氨酸甲基转移酶5
生发中心
效应器
生物
免疫学
调节器
卵泡期
细胞生物学
细胞
细胞因子
甲基转移酶
B细胞
遗传学
甲基化
基因
抗体
作者
Kaitlin A. Read,Stephanie A. Amici,Sadaf Farsi,Madeline P. Cutcliffe,Bella Lee,Chan-Wang Jerry Lio,Hao Wu,Mireia Guerau-de-Arellano,Kenneth J. Oestreich
标识
DOI:10.4049/jimmunol.2300270
摘要
Protein arginine methyltransferases (PRMTs) modify diverse protein targets and regulate numerous cellular processes; yet, their contributions to individual effector T cell responses during infections are incompletely understood. In this study, we identify PRMT5 as a critical regulator of CD4+ T follicular helper cell (Tfh) responses during influenza virus infection in mice. Conditional PRMT5 deletion in murine T cells results in an almost complete ablation of both Tfh and T follicular regulatory populations and, consequently, reduced B cell activation and influenza-specific Ab production. Supporting a potential mechanism, we observe elevated surface expression of IL-2Rα on non-T regulatory effector PRMT5-deficient T cells. Notably, IL-2 signaling is known to negatively impact Tfh differentiation. Collectively, our findings identify PRMT5 as a prominent regulator of Tfh programming, with potential causal links to IL-2 signaling.
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