IL17A and glomerulonephritis: In the BXD2 mouse model that recapitulates many SLE features like enhanced activation-induced cytidine deaminase (AICDA) activity, autoantibody generation, circulating immune complexes, and progressive glomerulonephritis, IL-17A has been shown to induce and stabilize autoreactive GC formation via B cell retention within GCs and increased CXCL12/CXCR4-mediated interactions between B cells and T cells resulting in AICDA upregulation and autoantibody generation [77–79].