Heterozygous Gnaq deficiency enhances Ifi202b/IFI16 and NF-κB activation in endothelial cells and exacerbates lupus nephritis pathology.

ABSTRACT: Lupus nephritis (LN), a severe complication of systemic lupus erythematosus (SLE), exhibits significant heterogeneity. Recent evidence suggests that non-immune factors contribute to end-organ damage, challenging the traditional view of LN solely arising from immune dysregulation. To investigate this, we employed autoimmune-prone Gnaq ^+/- mice receiving intraperitoneal pristane injections. Bone marrow transfer (BMT) distinguished the roles of immune versus non-immune cells. We observed that: (1) BMT from wild-type (WT) mice to Gnaq ^+/- recipients resulted in severe proteinuria and diffuse proliferative nephritis after pristane exposure; (2) GNAQ knockdown increased the expression of IFI16/Ifi202b and activated the NF-κB pathway in endothelial cells; and (

SUBMITTER: Zhang L 

PROVIDER: S-EPMC11301098 | biostudies-literature | 2024 Aug

REPOSITORIES: biostudies-literature