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Treg17 cells are programmed by Stat3 to suppress Th17 responses in systemic lupus

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Treg17 cells are programmed by Stat3 to suppress Th17 responses in systemic lupus. / Kluger, Malte A; Melderis, Simon; Nosko, Anna; Goerke, Boeren; Luig, Michael; Meyer, Matthias C; Turner, Jan-Eric; Meyer-Schwesinger, Catherine; Wegscheid, Claudia; Tiegs, Gisa; Stahl, Rolf A K; Panzer, Ulf; Steinmetz, Oliver M.

in: KIDNEY INT, Jahrgang 89, Nr. 1, 01.2016, S. 158-166.

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

Harvard

Kluger, MA, Melderis, S, Nosko, A, Goerke, B, Luig, M, Meyer, MC, Turner, J-E, Meyer-Schwesinger, C, Wegscheid, C, Tiegs, G, Stahl, RAK, Panzer, U & Steinmetz, OM 2016, 'Treg17 cells are programmed by Stat3 to suppress Th17 responses in systemic lupus', KIDNEY INT, Jg. 89, Nr. 1, S. 158-166. https://doi.org/10.1038/ki.2015.296

APA

Kluger, M. A., Melderis, S., Nosko, A., Goerke, B., Luig, M., Meyer, M. C., Turner, J-E., Meyer-Schwesinger, C., Wegscheid, C., Tiegs, G., Stahl, R. A. K., Panzer, U., & Steinmetz, O. M. (2016). Treg17 cells are programmed by Stat3 to suppress Th17 responses in systemic lupus. KIDNEY INT, 89(1), 158-166. https://doi.org/10.1038/ki.2015.296

Vancouver

Kluger MA, Melderis S, Nosko A, Goerke B, Luig M, Meyer MC et al. Treg17 cells are programmed by Stat3 to suppress Th17 responses in systemic lupus. KIDNEY INT. 2016 Jan;89(1):158-166. https://doi.org/10.1038/ki.2015.296

Bibtex

@article{ab31c803f20d4880b4b2609c6e661191,
title = "Treg17 cells are programmed by Stat3 to suppress Th17 responses in systemic lupus",
abstract = "Systemic lupus erythematosus (SLE) is a complex and potentially fatal autoimmune disorder. Although Th17 cells are thought to be central mediators of SLE, mechanisms underlying their counter regulation remain largely unknown. To help define this, we studied the function of the newly defined Stat3-dependent Th17-specific regulatory T cells (Treg17). Treg-specific deletion of Stat3 was achieved by generating Foxp3(Cre) × Stat3(fl/fl) mice and SLE was induced by intraperitoneal injection of pristane. Lack of Treg17 cells in these mice caused selectively enhanced peritoneal Th17 inflammation. Importantly, Treg17 deficiency also resulted in aggravated pulmonary vasculitis with increased percentages of Th17 cells and significantly higher mortality. Similarly, 4 and 9 months after pristane injection, analysis of renal and systemic immunity showed overshooting Th17 responses in the absence of Treg17 cells, associated with the aggravation of lupus nephritis. Expression of the Th17 characteristic trafficking receptor CCR6 was strikingly reduced on Tregs of Foxp3(Cre) × Stat3(fl/fl) mice, resulting in impaired renal Treg infiltration. Thus, Stat3-induced Treg17 cells are novel antiinflammatory mediators of SLE. One mechanism enabling Treg17 cells to target pathogenic Th17 responses is shared expression of the chemokine receptor CCR6.Kidney International advance online publication, 14 October 2015; doi:10.1038/ki.2015.296.",
author = "Kluger, {Malte A} and Simon Melderis and Anna Nosko and Boeren Goerke and Michael Luig and Meyer, {Matthias C} and Jan-Eric Turner and Catherine Meyer-Schwesinger and Claudia Wegscheid and Gisa Tiegs and Stahl, {Rolf A K} and Ulf Panzer and Steinmetz, {Oliver M}",
year = "2016",
month = jan,
doi = "10.1038/ki.2015.296",
language = "English",
volume = "89",
pages = "158--166",
journal = "KIDNEY INT",
issn = "0085-2538",
publisher = "NATURE PUBLISHING GROUP",
number = "1",

}

RIS

TY - JOUR

T1 - Treg17 cells are programmed by Stat3 to suppress Th17 responses in systemic lupus

AU - Kluger, Malte A

AU - Melderis, Simon

AU - Nosko, Anna

AU - Goerke, Boeren

AU - Luig, Michael

AU - Meyer, Matthias C

AU - Turner, Jan-Eric

AU - Meyer-Schwesinger, Catherine

AU - Wegscheid, Claudia

AU - Tiegs, Gisa

AU - Stahl, Rolf A K

AU - Panzer, Ulf

AU - Steinmetz, Oliver M

PY - 2016/1

Y1 - 2016/1

N2 - Systemic lupus erythematosus (SLE) is a complex and potentially fatal autoimmune disorder. Although Th17 cells are thought to be central mediators of SLE, mechanisms underlying their counter regulation remain largely unknown. To help define this, we studied the function of the newly defined Stat3-dependent Th17-specific regulatory T cells (Treg17). Treg-specific deletion of Stat3 was achieved by generating Foxp3(Cre) × Stat3(fl/fl) mice and SLE was induced by intraperitoneal injection of pristane. Lack of Treg17 cells in these mice caused selectively enhanced peritoneal Th17 inflammation. Importantly, Treg17 deficiency also resulted in aggravated pulmonary vasculitis with increased percentages of Th17 cells and significantly higher mortality. Similarly, 4 and 9 months after pristane injection, analysis of renal and systemic immunity showed overshooting Th17 responses in the absence of Treg17 cells, associated with the aggravation of lupus nephritis. Expression of the Th17 characteristic trafficking receptor CCR6 was strikingly reduced on Tregs of Foxp3(Cre) × Stat3(fl/fl) mice, resulting in impaired renal Treg infiltration. Thus, Stat3-induced Treg17 cells are novel antiinflammatory mediators of SLE. One mechanism enabling Treg17 cells to target pathogenic Th17 responses is shared expression of the chemokine receptor CCR6.Kidney International advance online publication, 14 October 2015; doi:10.1038/ki.2015.296.

AB - Systemic lupus erythematosus (SLE) is a complex and potentially fatal autoimmune disorder. Although Th17 cells are thought to be central mediators of SLE, mechanisms underlying their counter regulation remain largely unknown. To help define this, we studied the function of the newly defined Stat3-dependent Th17-specific regulatory T cells (Treg17). Treg-specific deletion of Stat3 was achieved by generating Foxp3(Cre) × Stat3(fl/fl) mice and SLE was induced by intraperitoneal injection of pristane. Lack of Treg17 cells in these mice caused selectively enhanced peritoneal Th17 inflammation. Importantly, Treg17 deficiency also resulted in aggravated pulmonary vasculitis with increased percentages of Th17 cells and significantly higher mortality. Similarly, 4 and 9 months after pristane injection, analysis of renal and systemic immunity showed overshooting Th17 responses in the absence of Treg17 cells, associated with the aggravation of lupus nephritis. Expression of the Th17 characteristic trafficking receptor CCR6 was strikingly reduced on Tregs of Foxp3(Cre) × Stat3(fl/fl) mice, resulting in impaired renal Treg infiltration. Thus, Stat3-induced Treg17 cells are novel antiinflammatory mediators of SLE. One mechanism enabling Treg17 cells to target pathogenic Th17 responses is shared expression of the chemokine receptor CCR6.Kidney International advance online publication, 14 October 2015; doi:10.1038/ki.2015.296.

U2 - 10.1038/ki.2015.296

DO - 10.1038/ki.2015.296

M3 - SCORING: Journal article

C2 - 26466322

VL - 89

SP - 158

EP - 166

JO - KIDNEY INT

JF - KIDNEY INT

SN - 0085-2538

IS - 1

ER -