NAT10-mediated acetylation of NIK mRNA in B cells promotes IgA production

ABSTRACT: The regulation of IgA expression is crucial for maintaining mucosal immune homeostasis, providing a vital defense mechanism against pathogens at mucosal surfaces. However, the intricate mechanisms regulating IgA class-switch recombination and its dysregulation in diseases such as inflammatory bowel disease remain a significant challenge in the field. In this study we analyse NAT10-dependent N4-acetylcytidine (ac4C) in NIK mRNA in B cells. We show that NAT10-mediated ac4C stabilizes NIK mRNA, thereby promoting IgA production, which is pivotal for immune defense. In a B-cell conditional NAT10 knockout mouse model we observe a reduction in IgA expression and a dampened noncanonical NF-B pathway, suggesting that NAT10 is a potential therapeutic target for IgA-related disorders. Taken together

SUBMITTER: Wan-jun Jiang 

PROVIDER: S-SCDT-10_1038-S44319-025-00509-2 | biostudies-other |

REPOSITORIES: biostudies-other