IL23A and ganglioneuroma: In this model, Th subset participation follows a biphasic pattern: early glomerular injury is dependent on Th17 cells, with GN effectively attenuated only during early disease in IL-23p19-deficient mice or following treatment with anti-IL-23p19 monoclonal antibody (mAb), whereas established GN relies on Th1-mediated inflammation and IL-12p35 (3).