T cell KAT6A deficiency relieves inflammatory bowel disease in mice.

ABSTRACT: The incidence of inflammatory bowel disease (IBD) has been increasing, and while the interaction between T cells and intestinal microorganisms is crucial in its pathogenesis, the related epigenetic mechanisms remain unclear. This study found that the expression of lysine acetyltransferase 6A (KAT6A) was increased in T cells of patients with acute colitis. Knocking out KAT6A in CD4⁺ T cells alleviated dextran sulfate sodium (DSS)-induced colitis in mice, as manifested in body weight, disease activity index, colon length, inflammation, and the expression of proinflammatory factors. Mechanistically, KAT6A deficiency upregulated the senescence of CD4⁺ T cells and affected the expression of related genes. Moreover, the regulation of colitis by CD4⁺ T cell KAT6A was dependent on the gut microbio

SUBMITTER: Huang SJ 

PROVIDER: S-EPMC12717716 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature