Regulatory T Cell-Derived IL-10 Ameliorates Crescentic GN.

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Regulatory T Cell-Derived IL-10 Ameliorates Crescentic GN. / Ostmann, Annett; Paust, Hans-Joachim; Panzer, Ulf; Wegscheid, Claudia; Kapffer, Sonja; Huber, Samuel; Flavell, Richard A; Erhardt, Annette; Tiegs, Gisa.

in: J AM SOC NEPHROL, Jahrgang 24, Nr. 6, 6, 2013, S. 930-942.

Publikationen: SCORING: Beitrag in Fachzeitschrift/ZeitungSCORING: ZeitschriftenaufsatzForschungBegutachtung

Harvard

Ostmann, A, Paust, H-J, Panzer, U, Wegscheid, C, Kapffer, S, Huber, S, Flavell, RA, Erhardt, A & Tiegs, G 2013, 'Regulatory T Cell-Derived IL-10 Ameliorates Crescentic GN.', J AM SOC NEPHROL, Jg. 24, Nr. 6, 6, S. 930-942. https://doi.org/10.1681/ASN.2012070684

APA

Ostmann, A., Paust, H-J., Panzer, U., Wegscheid, C., Kapffer, S., Huber, S., Flavell, R. A., Erhardt, A., & Tiegs, G. (2013). Regulatory T Cell-Derived IL-10 Ameliorates Crescentic GN. J AM SOC NEPHROL, 24(6), 930-942. [6]. https://doi.org/10.1681/ASN.2012070684

Vancouver

Bibtex

@article{22600ee7738b4b47882ac8976ea48730,
title = "Regulatory T Cell-Derived IL-10 Ameliorates Crescentic GN.",
abstract = "Regulatory T cells (Tregs) exert their immunosuppressive activity through several immunoregulatory mechanisms, including the production of anti-inflammatory cytokines such as IL-10. Although several studies suggest a role for Tregs in modulating crescentic GN, the underlying mechanisms are not well understood. Here, using IL-10 reporter mice, we detected IL-10-producing Foxp3(+) T cells in the kidney, blood, and secondary lymphoid tissue in a mouse model of crescentic GN. Specific inactivation of Il10 in Foxp3(+) Tregs eliminated the ability of these cells to suppress renal and systemic production of IFNγ and IL-17; these IL-10-deficient Tregs lost their capacity to attenuate renal tissue injury. These data highlight the suppressive functions of Tregs in crescentic GN and suggest the importance of Treg-derived IL-10 in ameliorating disease severity and in modulating both the Th1 and most notably Th17 immune response.",
keywords = "Animals, B-Lymphocytes, Blood Proteins, Dendritic Cells, Disease Models, Animal, Forkhead Transcription Factors, Glomerulonephritis, Interleukin-10, Kidney, Macrophages, Mice, Mice, Inbred C57BL, Mice, Knockout, RNA, Messenger, Severity of Illness Index, Sheep, Spleen, T-Lymphocytes, Regulatory, Th1 Cells, Th17 Cells",
author = "Annett Ostmann and Hans-Joachim Paust and Ulf Panzer and Claudia Wegscheid and Sonja Kapffer and Samuel Huber and Flavell, {Richard A} and Annette Erhardt and Gisa Tiegs",
year = "2013",
doi = "10.1681/ASN.2012070684",
language = "English",
volume = "24",
pages = "930--942",
journal = "J AM SOC NEPHROL",
issn = "1046-6673",
publisher = "American Society of Nephrology",
number = "6",

}

RIS

TY - JOUR

T1 - Regulatory T Cell-Derived IL-10 Ameliorates Crescentic GN.

AU - Ostmann, Annett

AU - Paust, Hans-Joachim

AU - Panzer, Ulf

AU - Wegscheid, Claudia

AU - Kapffer, Sonja

AU - Huber, Samuel

AU - Flavell, Richard A

AU - Erhardt, Annette

AU - Tiegs, Gisa

PY - 2013

Y1 - 2013

N2 - Regulatory T cells (Tregs) exert their immunosuppressive activity through several immunoregulatory mechanisms, including the production of anti-inflammatory cytokines such as IL-10. Although several studies suggest a role for Tregs in modulating crescentic GN, the underlying mechanisms are not well understood. Here, using IL-10 reporter mice, we detected IL-10-producing Foxp3(+) T cells in the kidney, blood, and secondary lymphoid tissue in a mouse model of crescentic GN. Specific inactivation of Il10 in Foxp3(+) Tregs eliminated the ability of these cells to suppress renal and systemic production of IFNγ and IL-17; these IL-10-deficient Tregs lost their capacity to attenuate renal tissue injury. These data highlight the suppressive functions of Tregs in crescentic GN and suggest the importance of Treg-derived IL-10 in ameliorating disease severity and in modulating both the Th1 and most notably Th17 immune response.

AB - Regulatory T cells (Tregs) exert their immunosuppressive activity through several immunoregulatory mechanisms, including the production of anti-inflammatory cytokines such as IL-10. Although several studies suggest a role for Tregs in modulating crescentic GN, the underlying mechanisms are not well understood. Here, using IL-10 reporter mice, we detected IL-10-producing Foxp3(+) T cells in the kidney, blood, and secondary lymphoid tissue in a mouse model of crescentic GN. Specific inactivation of Il10 in Foxp3(+) Tregs eliminated the ability of these cells to suppress renal and systemic production of IFNγ and IL-17; these IL-10-deficient Tregs lost their capacity to attenuate renal tissue injury. These data highlight the suppressive functions of Tregs in crescentic GN and suggest the importance of Treg-derived IL-10 in ameliorating disease severity and in modulating both the Th1 and most notably Th17 immune response.

KW - Animals

KW - B-Lymphocytes

KW - Blood Proteins

KW - Dendritic Cells

KW - Disease Models, Animal

KW - Forkhead Transcription Factors

KW - Glomerulonephritis

KW - Interleukin-10

KW - Kidney

KW - Macrophages

KW - Mice

KW - Mice, Inbred C57BL

KW - Mice, Knockout

KW - RNA, Messenger

KW - Severity of Illness Index

KW - Sheep

KW - Spleen

KW - T-Lymphocytes, Regulatory

KW - Th1 Cells

KW - Th17 Cells

U2 - 10.1681/ASN.2012070684

DO - 10.1681/ASN.2012070684

M3 - SCORING: Journal article

C2 - 23641052

VL - 24

SP - 930

EP - 942

JO - J AM SOC NEPHROL

JF - J AM SOC NEPHROL

SN - 1046-6673

IS - 6

M1 - 6

ER -