Butyrophilin 3A1 Contributes to Inflammation and Induces a Lupus-Like Disease by Inhibiting the IL-38-Ferroptosis Axis.

ABSTRACT: Systemic lupus erythematosus (SLE) is an autoimmune disease of unknown origin. Recent evidence has linked butyrophilin 3A1 (BTN3A1) to immune dysregulation. This study was to elucidate the relationship of BTN3A1 in SLE. Expression of BTN3A1 in plasma and peripheral blood mononuclear cells from SLE patients and healthy controls explored the association between BTN3A1 and SLE. We found that BTN3A1 mRNA, plasma levels, and expression in CD4⁺ T cells were significantly elevated in SLE patients. In BTN3A1 gene knock-in (BTN3A1^KI) mice, inflammation and lupus-like manifestations occurred, including increased proportions of Th1, Th2, and Th17 cells, decreased Treg cells, elevated levels of inflammatory cytokines and anti-dsDNA antibodies, renal injury, and suppressed IL-38 s

SUBMITTER: Xu WD 

PROVIDER: S-EPMC12433891 | biostudies-literature | 2025 Sep

REPOSITORIES: biostudies-literature