RNA m⁶A methylation writers in autoimmune diseases: structure, function, and therapeutic opportunities

N⁶-methyladenosine (m⁶A) is the most abundant internal modification of eukaryotic mRNA, and its dysregulation is increasingly linked to autoimmune diseases. Unlike previous reviews that broadly cover the entire m⁶A network, this review adopts an m⁶A writer centric perspective. The m⁶A writer complex serves as the upstream gatekeeper of epitranscriptomic regulation. We summarize its structural organization and cell‑type‑specific functions in controlling immune cell differentiation and function, as well as its protective roles in parenchymal tissues. Accumulating evidence shows that the writer complex exerts context‑dependent dual actions across a wide range of autoimmune conditions, including rheumatoid arthritis, lupus, psoriasis, and others. We also discuss the mechanistic basis of this functional heterogeneity, involving microenvironmental signals, subunit composition, and reader proteins. Notably, our review not only focuses on the roles and mechanisms of writer‑mediated m⁶A modification in various immune cells but also summarizes its pharmacological modulators, which represents a key advantage over previous reviews. By focusing specifically on the writer complex, we provide a more proximal and mechanistically feasible framework for precise epitranscriptomic intervention in autoimmune disorders.