RNA N⁶-methyladenosine reader protein YTHDF1 promotes plasma cell differentiation via IRF4 regulation in systemic lupus erythematosus.

ABSTRACT: B cell malfunction is implicated in the pathogenesis of systemic lupus erythematosus (SLE) through the release of proinflammatory cytokines and the production of autoreactive antibodies. RNA N⁶-methyladenosine (m⁶A) is the predominant post-transcriptional RNA modification that has been reported to control various biological processes. Whether RNA m⁶A alteration and m⁶A reader protein YTHDF1 contribute to B cell activation and terminal B cell differentiation in SLE has not been fully demonstrated. Here we observed that SLE peripheral B cell subsets, activated B cells and differentiated plasma cells (PCs) had abnormally elevated levels of YTHDF1, the deficit of which attenuated PC differentiation both in vitro and in mouse models that have been imm

SUBMITTER: Lu S 

PROVIDER: S-EPMC12686027 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature