Acetylation in autoimmune diseases: From mechanistic insights to therapeutic prospects

Autoimmune diseases arise from a breakdown of immune tolerance, leading to sustained inflammation and tissue damage. Increasing evidence indicates that epigenetic dysregulation contributes to this loss of tolerance. Among diverse epigenetic mechanisms, protein and RNA acetylation/deacetylation have emerged as pivotal modulators of immune cell activation, differentiation, and effector function. Aberrant acetylation of histone and non-histone proteins has been implicated in shaping pathogenic immune responses across multiple autoimmune disorders. Concurrently, a substantial body of research has focused on RNA-level acetylation in autoimmune diseases. This review summarizes the effects of acetylation/deacetylaton modifications on immune cells, their dysregulated patterns across autoimmune diseases, and the existing clinical research in autoimmune field. Together, these insights provide a conceptual framework for linking acetylation modification to immune imbalance and point toward new avenues for precision therapy in autoimmune diseases.