Cxcl9^high macrophages recruit circulating Cxcr3+ plasmablasts into kidneys to promote pathogenesis of lupus nephritis mice.

ABSTRACT: Systemic lupus erythematosus (SLE) is an autoimmune disease driven by autoantibody production. Lupus nephritis (LN), a severe SLE complication, is primarily caused by renal autoantibodies. Long-lived plasma cells (LLPCs), the main producers of these autoantibodies, are especially elevated in the kidney of LN patients, particularly in refractory or recurrent cases. However, the cause of increased LLPCs in LN kidneys remains unknown. This study uses an LN mouse model and combines single-cell RNA sequencing with spatial transcriptomics, finding that kidney-resident Cxcl9^high macrophages and their secreted chemokine Cxcl9 significantly rise with disease progression. This increase in Cxcl9 attracts Cxcr3+ plasmablasts in peripheral blood into the kidneys, where they differentiate int

SUBMITTER: Zhao J 

PROVIDER: S-EPMC12511401 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature