Of note, during early stages of experimental GN, γδ T cells are the major cellular source of IL-17A in the kidney but at later stages CD4+ TH17 cell-derived IL-17A drives CXCL5 expression in kidney tubular cells, leading to recruitment of CXCR2+ neutrophils that contribute to renal tissue injury (Disteldorf et al. 2015; Turner et al. 2012a, b). This evidence concerns the gene IL17A and ganglioneuroma.