Table 1.

Role of chemokine receptor pathways for T cell trafficking and function in immune-mediated kidney diseases

T cell subsets	Chemokine receptor/main ligand(s)	Axis function/disease
TH1 cells	CCR5–CCL3-5 CXCR3–CXCL9-11	Deletion of CCR5 resulted in both pro- and anti-inflammatory responses in various GN models, most probably via upregulation of an alternative chemokine/chemokine receptor pathway (Anders et al. 2003; Panzer et al. 1999; Turner et al. 2012a, b; Turner et al. 2008) CXCR3 targeting resulted in impaired trafficking of pathogenic TH1 cells and an ameliorated course of crescentic and proliferative GN (Menke et al. 2008; Panzer et al. 2007; Steinmetz et al. 2009). In humans CXCR3+ T cells are recruited into inflamed kidneys, are enriched in urine and might be a biomarker of nephritis activity in SLE (Enghard et al. 2009)
TH17 cells	CCR6–CCL20	CCR6 is highly expressed on human and mouse TH17 cells. CCR6+ TH17 are enriched in the kidney of ANCA-GN patients (Krebs et al. 2016; Krebs et al. 2020). In experimental crescentic GN (NTN) CCR6+ TH17 are recruited via CCL20 into the inflamed kidney (Turner et al. 2010)
TH2 cells	CCR4–CCL17, CCL21 CCR8–CCL18	CCR4+ T lymphocytes in peripheral blood, which represent Th2 cells, preferentially migrate into the renal tissue of patients with lupus nephritis (Yamada et al. 2002) Targeting of CCL18/CCR8 had no major impact of TH2 response in experimental crescentic GN but reduced the infiltration of pathogenic mononuclear phagocyte and could serve as a biomarker for disease activity and renal relapse in ANCA-associated crescentic GN (Brix et al. 2015)
Tregs	CCR6–CCL20 CCR7–CCL19, CCL21 CXCR3–CXCL9-11	Stat3 activation leads to CCR6 expression on Tregs in mice and humans, which mediates specific control of TH17 immunity in several forms of experimental GNs (Kluger et al. 2014; Kluger et al. 2016; Turner et al. 2010) CCR7 deficiency exacerbates injury in crescentic GN due to aberrant localization of regulatory T cells (Eller et al. 2010) Tbet activation leads to CXCR3 expression on Tregs and mediates specific control of TH1 immunity (Nosko et al. 2017). Tregs expressing CXCR3 are enriched in the kidneys of patients with ANCA-associated crescentic GN and co-localize with CXCR3+ effector T cells (Paust et al. 2016)
T follicular helper (TFH) cells	CXCR5–CXCL15	CXCR5 is a marker for TFH cells and promotes aberrant germinal center responses via IL-21 production with autoreactive memory B cell development and plasma cell-derived autoantibody production in SLE (Choi et al. 2017)
Natural killer T (NKT) cells	CXCR6–CXCL16	More than 90% of renal invariant NKT cells expressed CXCR6 and renal DCs produced high amounts of the cognate ligand CXCL16 in GN, suggesting that renal DC-derived CXCL16 might attract protective CXCR6+ invariant NKT cells (Riedel et al. 2012)