Th17 cells express interleukin-10 receptor and are controlled by Foxp3⁻ and Foxp3+ regulatory CD4+ T cells in an interleukin-10-dependent manner

Standard

Th17 cells express interleukin-10 receptor and are controlled by Foxp3⁻ and Foxp3+ regulatory CD4+ T cells in an interleukin-10-dependent manner. / Huber, Samuel; Gagliani, Nicola; Esplugues, Enric; O'Connor, William; Huber, Francis J; Chaudhry, Ashutosh; Kamanaka, Masahito; Kobayashi, Yasushi; Booth, Carmen J; Rudensky, Alexander Y; Roncarolo, Maria Grazia; Battaglia, Manuela; Flavell, Richard A.

In: IMMUNITY, Vol. 34, No. 4, 4, 22.04.2011, p. 554-565.

Research output: SCORING: Contribution to journalSCORING: Journal articleResearchpeer-review

Harvard

Huber, S, Gagliani, N, Esplugues, E, O'Connor, W, Huber, FJ, Chaudhry, A, Kamanaka, M, Kobayashi, Y, Booth, CJ, Rudensky, AY, Roncarolo, MG, Battaglia, M & Flavell, RA 2011, 'Th17 cells express interleukin-10 receptor and are controlled by Foxp3⁻ and Foxp3+ regulatory CD4+ T cells in an interleukin-10-dependent manner', IMMUNITY, vol. 34, no. 4, 4, pp. 554-565. https://doi.org/10.1016/j.immuni.2011.01.020

APA

Huber, S., Gagliani, N., Esplugues, E., O'Connor, W., Huber, F. J., Chaudhry, A., Kamanaka, M., Kobayashi, Y., Booth, C. J., Rudensky, A. Y., Roncarolo, M. G., Battaglia, M., & Flavell, R. A. (2011). Th17 cells express interleukin-10 receptor and are controlled by Foxp3⁻ and Foxp3+ regulatory CD4+ T cells in an interleukin-10-dependent manner. IMMUNITY, 34(4), 554-565. [4]. https://doi.org/10.1016/j.immuni.2011.01.020

Vancouver

Bibtex

@article{a109585dcc5641578c2d907bd21a58a4,
title = "Th17 cells express interleukin-10 receptor and are controlled by Foxp3⁻ and Foxp3+ regulatory CD4+ T cells in an interleukin-10-dependent manner",
abstract = "T helper 17 (Th17) cells are important for host defense against extracellular microorganisms. However, they are also implicated in autoimmune and chronic inflammatory diseases, and as such need to be tightly regulated. The mechanisms that directly control committed pathogenic Th17 cells in vivo remain unclear. We showed here that IL-17A-producing CD4+ T cells expressed interleukin-10 receptor ? (IL-10R?) in vivo. Importantly, T cell-specific blockade of IL-10 signaling led to a selective increase of IL-17A+IFN-?? (Th17) and IL-17A+IFN-?+ (Th17+Th1) CD4+ T cells during intestinal inflammation in the small intestine. CD4+Foxp3? IL-10-producing (Tr1) cells and CD4+Foxp3+ regulatory (Treg) cells were able to control Th17 and Th17+Th1 cells in an IL-10-dependent manner in vivo. Lastly, IL-10 treatment of mice with established colitis decreased Th17 and Th17+Th1 cell frequencies via direct signaling in T cells. Thus, IL-10 signaling directly suppresses Th17 and Th17+Th1 cells.",
keywords = "Animals, Disease Progression, Mice, Mice, Inbred C57BL, Signal Transduction, Cell Proliferation, Interferon-gamma/immunology, CD4-Positive T-Lymphocytes/cytology/*immunology/metabolism, Colitis/immunology/pathology, Forkhead Transcription Factors/immunology, Interleukin-10/*immunology/metabolism, Interleukin-10 Receptor alpha Subunit/*immunology/metabolism, Peptide Fragments/immunology, Th17 Cells/cytology/*immunology/metabolism, Animals, Disease Progression, Mice, Mice, Inbred C57BL, Signal Transduction, Cell Proliferation, Interferon-gamma/immunology, CD4-Positive T-Lymphocytes/cytology/*immunology/metabolism, Colitis/immunology/pathology, Forkhead Transcription Factors/immunology, Interleukin-10/*immunology/metabolism, Interleukin-10 Receptor alpha Subunit/*immunology/metabolism, Peptide Fragments/immunology, Th17 Cells/cytology/*immunology/metabolism",
author = "Samuel Huber and Nicola Gagliani and Enric Esplugues and William O'Connor and Huber, {Francis J} and Ashutosh Chaudhry and Masahito Kamanaka and Yasushi Kobayashi and Booth, {Carmen J} and Rudensky, {Alexander Y} and Roncarolo, {Maria Grazia} and Manuela Battaglia and Flavell, {Richard A}",
note = "Copyright {\textcopyright} 2011 Elsevier Inc. All rights reserved.",
year = "2011",
month = apr,
day = "22",
doi = "10.1016/j.immuni.2011.01.020",
language = "English",
volume = "34",
pages = "554--565",
journal = "IMMUNITY",
issn = "1074-7613",
publisher = "Cell Press",
number = "4",

}

RIS

TY - JOUR

T1 - Th17 cells express interleukin-10 receptor and are controlled by Foxp3⁻ and Foxp3+ regulatory CD4+ T cells in an interleukin-10-dependent manner

AU - Huber, Samuel

AU - Gagliani, Nicola

AU - Esplugues, Enric

AU - O'Connor, William

AU - Huber, Francis J

AU - Chaudhry, Ashutosh

AU - Kamanaka, Masahito

AU - Kobayashi, Yasushi

AU - Booth, Carmen J

AU - Rudensky, Alexander Y

AU - Roncarolo, Maria Grazia

AU - Battaglia, Manuela

AU - Flavell, Richard A

N1 - Copyright © 2011 Elsevier Inc. All rights reserved.

PY - 2011/4/22

Y1 - 2011/4/22

N2 - T helper 17 (Th17) cells are important for host defense against extracellular microorganisms. However, they are also implicated in autoimmune and chronic inflammatory diseases, and as such need to be tightly regulated. The mechanisms that directly control committed pathogenic Th17 cells in vivo remain unclear. We showed here that IL-17A-producing CD4+ T cells expressed interleukin-10 receptor ? (IL-10R?) in vivo. Importantly, T cell-specific blockade of IL-10 signaling led to a selective increase of IL-17A+IFN-?? (Th17) and IL-17A+IFN-?+ (Th17+Th1) CD4+ T cells during intestinal inflammation in the small intestine. CD4+Foxp3? IL-10-producing (Tr1) cells and CD4+Foxp3+ regulatory (Treg) cells were able to control Th17 and Th17+Th1 cells in an IL-10-dependent manner in vivo. Lastly, IL-10 treatment of mice with established colitis decreased Th17 and Th17+Th1 cell frequencies via direct signaling in T cells. Thus, IL-10 signaling directly suppresses Th17 and Th17+Th1 cells.

AB - T helper 17 (Th17) cells are important for host defense against extracellular microorganisms. However, they are also implicated in autoimmune and chronic inflammatory diseases, and as such need to be tightly regulated. The mechanisms that directly control committed pathogenic Th17 cells in vivo remain unclear. We showed here that IL-17A-producing CD4+ T cells expressed interleukin-10 receptor ? (IL-10R?) in vivo. Importantly, T cell-specific blockade of IL-10 signaling led to a selective increase of IL-17A+IFN-?? (Th17) and IL-17A+IFN-?+ (Th17+Th1) CD4+ T cells during intestinal inflammation in the small intestine. CD4+Foxp3? IL-10-producing (Tr1) cells and CD4+Foxp3+ regulatory (Treg) cells were able to control Th17 and Th17+Th1 cells in an IL-10-dependent manner in vivo. Lastly, IL-10 treatment of mice with established colitis decreased Th17 and Th17+Th1 cell frequencies via direct signaling in T cells. Thus, IL-10 signaling directly suppresses Th17 and Th17+Th1 cells.

KW - Animals

KW - Disease Progression

KW - Mice

KW - Mice, Inbred C57BL

KW - Signal Transduction

KW - Cell Proliferation

KW - Interferon-gamma/immunology

KW - CD4-Positive T-Lymphocytes/cytology/immunology/metabolism

KW - Colitis/immunology/pathology

KW - Forkhead Transcription Factors/immunology

KW - Interleukin-10/immunology/metabolism

KW - Interleukin-10 Receptor alpha Subunit/immunology/metabolism

KW - Peptide Fragments/immunology

KW - Th17 Cells/cytology/immunology/metabolism

KW - Animals

KW - Disease Progression

KW - Mice

KW - Mice, Inbred C57BL

KW - Signal Transduction

KW - Cell Proliferation

KW - Interferon-gamma/immunology

KW - CD4-Positive T-Lymphocytes/cytology/immunology/metabolism

KW - Colitis/immunology/pathology

KW - Forkhead Transcription Factors/immunology

KW - Interleukin-10/immunology/metabolism

KW - Interleukin-10 Receptor alpha Subunit/immunology/metabolism

KW - Peptide Fragments/immunology

KW - Th17 Cells/cytology/immunology/metabolism

U2 - 10.1016/j.immuni.2011.01.020

DO - 10.1016/j.immuni.2011.01.020

M3 - SCORING: Journal article

C2 - 21511184

VL - 34

SP - 554

EP - 565

JO - IMMUNITY

JF - IMMUNITY

SN - 1074-7613

IS - 4

M1 - 4

ER -