Immature renal dendritic cells recruit regulatory CXCR6(+) invariant natural killer T cells to attenuate crescentic GN.
Standard
Immature renal dendritic cells recruit regulatory CXCR6(+) invariant natural killer T cells to attenuate crescentic GN. / Riedel, Jan-Hendrik; Paust, Hans-Joachim; Turner, Jan Eric; Tittel, André P; Krebs, Christian; Disteldorf, Erik; Wegscheid, Claudia; Tiegs, Gisa; Velden, Joachim; Mittrücker, Hans Willi; Garbi, Natalio; Stahl, Rolf A.K.; Steinmetz, Oliver; Kurts, Christian; Panzer, Ulf.
In: J AM SOC NEPHROL, Vol. 23, No. 12, 12, 2012, p. 1987-2000.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
Harvard
APA
Vancouver
Bibtex
}
RIS
TY - JOUR
T1 - Immature renal dendritic cells recruit regulatory CXCR6(+) invariant natural killer T cells to attenuate crescentic GN.
AU - Riedel, Jan-Hendrik
AU - Paust, Hans-Joachim
AU - Turner, Jan Eric
AU - Tittel, André P
AU - Krebs, Christian
AU - Disteldorf, Erik
AU - Wegscheid, Claudia
AU - Tiegs, Gisa
AU - Velden, Joachim
AU - Mittrücker, Hans Willi
AU - Garbi, Natalio
AU - Stahl, Rolf A.K.
AU - Steinmetz, Oliver
AU - Kurts, Christian
AU - Panzer, Ulf
PY - 2012
Y1 - 2012
N2 - Immature renal dendritic cells (DCs) are protective early in murine crescentic GN, but the mechanisms underlying this protection are unknown. Here, depletion of DCs reduced the recruitment of invariant natural killer T (iNKT) cells, which attenuate GN, into the kidney in the early stage of experimental crescentic GN. More than 90% of renal iNKT cells expressed the chemokine receptor CXCR6, and renal DCs produced high amounts of the cognate ligand CXCL16 early after induction of nephritis, suggesting that renal DC-derived CXCL16 might attract protective CXCR6(+) iNKT cells. Consistent with this finding, CXCR6-deficient mice exhibited less iNKT cell recruitment and developed nephritis that was more severe, similar to the aggravated nephritis observed in mice depleted of immature DCs. Finally, adoptive transfer of CXCR6-competent NKT cells ameliorated nephritis. Taken together, these results suggest an immunoprotective mechanism involving immature DCs, CXCL16, CXCR6, and regulatory iNKT cells, which might stimulate the development of new therapeutic strategies for GN.
AB - Immature renal dendritic cells (DCs) are protective early in murine crescentic GN, but the mechanisms underlying this protection are unknown. Here, depletion of DCs reduced the recruitment of invariant natural killer T (iNKT) cells, which attenuate GN, into the kidney in the early stage of experimental crescentic GN. More than 90% of renal iNKT cells expressed the chemokine receptor CXCR6, and renal DCs produced high amounts of the cognate ligand CXCL16 early after induction of nephritis, suggesting that renal DC-derived CXCL16 might attract protective CXCR6(+) iNKT cells. Consistent with this finding, CXCR6-deficient mice exhibited less iNKT cell recruitment and developed nephritis that was more severe, similar to the aggravated nephritis observed in mice depleted of immature DCs. Finally, adoptive transfer of CXCR6-competent NKT cells ameliorated nephritis. Taken together, these results suggest an immunoprotective mechanism involving immature DCs, CXCL16, CXCR6, and regulatory iNKT cells, which might stimulate the development of new therapeutic strategies for GN.
KW - Animals
KW - Male
KW - Mice
KW - Mice, Inbred C57BL
KW - Sheep
KW - Glomerulonephritis/immunology
KW - Chemokine CXCL6/metabolism
KW - Dendritic Cells/physiology
KW - Leukocytes, Mononuclear/physiology
KW - Receptors, CXCR/metabolism
KW - Animals
KW - Male
KW - Mice
KW - Mice, Inbred C57BL
KW - Sheep
KW - Glomerulonephritis/immunology
KW - Chemokine CXCL6/metabolism
KW - Dendritic Cells/physiology
KW - Leukocytes, Mononuclear/physiology
KW - Receptors, CXCR/metabolism
M3 - SCORING: Journal article
VL - 23
SP - 1987
EP - 2000
JO - J AM SOC NEPHROL
JF - J AM SOC NEPHROL
SN - 1046-6673
IS - 12
M1 - 12
ER -
