In the kidney, Th17 effector cells have been demonstrated in biopsy samples in human glomerulonephritis (Abdulahad et al. 2009) and may participate in the pathogenesis of proliferative glomerulonephritis via production of IL-17 and direct induction of renal inflammation (Kim et al. 2009; Miossec et al. 2009; Turner et al. 2010; Kitching and Holdsworth 2011). Recent studies utilizing genetically engineered mice showed that RORγt promotes the development of crescentic glomerulonephritis by directing nephritogenic Th17 responses (Steinmetz et al. 2011) . In contrast, the adaptive immune response by T cells is regulated by T regulatory cell (Treg)s (Jiang and Chess 2006). Treg cells are in charge of suppressing potentially deleterious activities.
