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Autoimmune Renal Disease Is Exacerbated by S1P-Receptor-1-Dependent Intestinal Th17 Cell Migration to the Kidney

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Autoimmune Renal Disease Is Exacerbated by S1P-Receptor-1-Dependent Intestinal Th17 Cell Migration to the Kidney. / Krebs, Christian F; Paust, Hans-Joachim; Krohn, Sonja; Koyro, Tobias; Brix, Silke R; Riedel, Jan-Hendrik; Bartsch, Patricia; Wiech, Thorsten; Meyer-Schwesinger, Catherine; Huang, Jiabin; Fischer, Nicole; Busch, Christoph Philipp; Mittrücker, Hans-Willi; Steinhoff, Ulrich; Stockinger, Brigitta; Perez, Laura Garcia; Wenzel, Ulrich O; Janneck, Matthias; Steinmetz, Oliver M; Gagliani, Nicola; Stahl, Rolf A K; Huber, Samuel; Turner, Jan-Eric; Panzer, Ulf.

in: IMMUNITY, Jahrgang 45, Nr. 5, 15.11.2016, S. 1078-1092.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Krebs, CF, Paust, H-J, Krohn, S, Koyro, T, Brix, SR, Riedel, J-H, Bartsch, P, Wiech, T, Meyer-Schwesinger, C, Huang, J, Fischer, N, Busch, CP, Mittrücker, H-W, Steinhoff, U, Stockinger, B, Perez, LG, Wenzel, UO, Janneck, M, Steinmetz, OM, Gagliani, N, Stahl, RAK, Huber, S, Turner, J-E & Panzer, U 2016, 'Autoimmune Renal Disease Is Exacerbated by S1P-Receptor-1-Dependent Intestinal Th17 Cell Migration to the Kidney', IMMUNITY, Jg. 45, Nr. 5, S. 1078-1092. https://doi.org/10.1016/j.immuni.2016.10.020

APA

Krebs, C. F., Paust, H-J., Krohn, S., Koyro, T., Brix, S. R., Riedel, J-H., Bartsch, P., Wiech, T., Meyer-Schwesinger, C., Huang, J., Fischer, N., Busch, C. P., Mittrücker, H-W., Steinhoff, U., Stockinger, B., Perez, L. G., Wenzel, U. O., Janneck, M., Steinmetz, O. M., ... Panzer, U. (2016). Autoimmune Renal Disease Is Exacerbated by S1P-Receptor-1-Dependent Intestinal Th17 Cell Migration to the Kidney. IMMUNITY, 45(5), 1078-1092. https://doi.org/10.1016/j.immuni.2016.10.020

Vancouver

Krebs CF, Paust H-J, Krohn S, Koyro T, Brix SR, Riedel J-H et al. Autoimmune Renal Disease Is Exacerbated by S1P-Receptor-1-Dependent Intestinal Th17 Cell Migration to the Kidney. IMMUNITY. 2016 Nov 15;45(5):1078-1092. https://doi.org/10.1016/j.immuni.2016.10.020

Bibtex

@article{3730964a0c4a41f58967b564e0c417bc,
title = "Autoimmune Renal Disease Is Exacerbated by S1P-Receptor-1-Dependent Intestinal Th17 Cell Migration to the Kidney",
abstract = "Th17 cells are most abundant in the gut, where their presence depends on the intestinal microbiota. Here, we examined whether intestinal Th17 cells contribute to extra-intestinal Th17 responses in autoimmune kidney disease. We found high frequencies of Th17 cells in the kidneys of patients with antineutrophil cytoplasmatic antibody (ANCA)-associated glomerulonephritis. We utilized photoconversion of intestinal cells in Kaede mice to track intestinal T cell mobilization upon glomerulonephritis induction, and we found that Th17 cells egress from the gut in a S1P-receptor-1-dependent fashion and subsequently migrate to the kidney via the CCL20/CCR6 axis. Depletion of intestinal Th17 cells in germ-free and antibiotic-treated mice ameliorated renal disease, whereas expansion of these cells upon Citrobacter rodentium infection exacerbated pathology. Thus, in some autoimmune settings, intestinal Th17 cells migrate into target organs, where they contribute to pathology. Targeting the intestinal Th17 cell {"}reservoir{"} may present a therapeutic strategy for these autoimmune disorders.POM-Newsletter",
author = "Krebs, {Christian F} and Hans-Joachim Paust and Sonja Krohn and Tobias Koyro and Brix, {Silke R} and Jan-Hendrik Riedel and Patricia Bartsch and Thorsten Wiech and Catherine Meyer-Schwesinger and Jiabin Huang and Nicole Fischer and Busch, {Christoph Philipp} and Hans-Willi Mittr{\"u}cker and Ulrich Steinhoff and Brigitta Stockinger and Perez, {Laura Garcia} and Wenzel, {Ulrich O} and Matthias Janneck and Steinmetz, {Oliver M} and Nicola Gagliani and Stahl, {Rolf A K} and Samuel Huber and Jan-Eric Turner and Ulf Panzer",
note = "Copyright {\textcopyright} 2016 The Authors. Published by Elsevier Inc. All rights reserved.",
year = "2016",
month = nov,
day = "15",
doi = "10.1016/j.immuni.2016.10.020",
language = "English",
volume = "45",
pages = "1078--1092",
journal = "IMMUNITY",
issn = "1074-7613",
publisher = "Cell Press",
number = "5",

}

RIS

TY - JOUR

T1 - Autoimmune Renal Disease Is Exacerbated by S1P-Receptor-1-Dependent Intestinal Th17 Cell Migration to the Kidney

AU - Krebs, Christian F

AU - Paust, Hans-Joachim

AU - Krohn, Sonja

AU - Koyro, Tobias

AU - Brix, Silke R

AU - Riedel, Jan-Hendrik

AU - Bartsch, Patricia

AU - Wiech, Thorsten

AU - Meyer-Schwesinger, Catherine

AU - Huang, Jiabin

AU - Fischer, Nicole

AU - Busch, Christoph Philipp

AU - Mittrücker, Hans-Willi

AU - Steinhoff, Ulrich

AU - Stockinger, Brigitta

AU - Perez, Laura Garcia

AU - Wenzel, Ulrich O

AU - Janneck, Matthias

AU - Steinmetz, Oliver M

AU - Gagliani, Nicola

AU - Stahl, Rolf A K

AU - Huber, Samuel

AU - Turner, Jan-Eric

AU - Panzer, Ulf

N1 - Copyright © 2016 The Authors. Published by Elsevier Inc. All rights reserved.

PY - 2016/11/15

Y1 - 2016/11/15

N2 - Th17 cells are most abundant in the gut, where their presence depends on the intestinal microbiota. Here, we examined whether intestinal Th17 cells contribute to extra-intestinal Th17 responses in autoimmune kidney disease. We found high frequencies of Th17 cells in the kidneys of patients with antineutrophil cytoplasmatic antibody (ANCA)-associated glomerulonephritis. We utilized photoconversion of intestinal cells in Kaede mice to track intestinal T cell mobilization upon glomerulonephritis induction, and we found that Th17 cells egress from the gut in a S1P-receptor-1-dependent fashion and subsequently migrate to the kidney via the CCL20/CCR6 axis. Depletion of intestinal Th17 cells in germ-free and antibiotic-treated mice ameliorated renal disease, whereas expansion of these cells upon Citrobacter rodentium infection exacerbated pathology. Thus, in some autoimmune settings, intestinal Th17 cells migrate into target organs, where they contribute to pathology. Targeting the intestinal Th17 cell "reservoir" may present a therapeutic strategy for these autoimmune disorders.POM-Newsletter

AB - Th17 cells are most abundant in the gut, where their presence depends on the intestinal microbiota. Here, we examined whether intestinal Th17 cells contribute to extra-intestinal Th17 responses in autoimmune kidney disease. We found high frequencies of Th17 cells in the kidneys of patients with antineutrophil cytoplasmatic antibody (ANCA)-associated glomerulonephritis. We utilized photoconversion of intestinal cells in Kaede mice to track intestinal T cell mobilization upon glomerulonephritis induction, and we found that Th17 cells egress from the gut in a S1P-receptor-1-dependent fashion and subsequently migrate to the kidney via the CCL20/CCR6 axis. Depletion of intestinal Th17 cells in germ-free and antibiotic-treated mice ameliorated renal disease, whereas expansion of these cells upon Citrobacter rodentium infection exacerbated pathology. Thus, in some autoimmune settings, intestinal Th17 cells migrate into target organs, where they contribute to pathology. Targeting the intestinal Th17 cell "reservoir" may present a therapeutic strategy for these autoimmune disorders.POM-Newsletter

U2 - 10.1016/j.immuni.2016.10.020

DO - 10.1016/j.immuni.2016.10.020

M3 - SCORING: Journal article

C2 - 27851911

VL - 45

SP - 1078

EP - 1092

JO - IMMUNITY

JF - IMMUNITY

SN - 1074-7613

IS - 5

ER -