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MyD88 signalling in colonic mononuclear phagocytes drives colitis in IL-10-deficient mice

Standard

MyD88 signalling in colonic mononuclear phagocytes drives colitis in IL-10-deficient mice. / Hoshi, Namiko; Schenten, Dominik; Nish, Simone A; Walther, Zenta; Gagliani, Nicola; Flavell, Richard A; Reizis, Boris; Shen, Zeli; Fox, James G; Iwasaki, Akiko; Medzhitov, Ruslan.

in: NAT COMMUN, Jahrgang 3, 2012, S. 1120.

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

Harvard

Hoshi, N, Schenten, D, Nish, SA, Walther, Z, Gagliani, N, Flavell, RA, Reizis, B, Shen, Z, Fox, JG, Iwasaki, A & Medzhitov, R 2012, 'MyD88 signalling in colonic mononuclear phagocytes drives colitis in IL-10-deficient mice', NAT COMMUN, Jg. 3, S. 1120. https://doi.org/10.1038/ncomms2113

APA

Hoshi, N., Schenten, D., Nish, S. A., Walther, Z., Gagliani, N., Flavell, R. A., Reizis, B., Shen, Z., Fox, J. G., Iwasaki, A., & Medzhitov, R. (2012). MyD88 signalling in colonic mononuclear phagocytes drives colitis in IL-10-deficient mice. NAT COMMUN, 3, 1120. https://doi.org/10.1038/ncomms2113

Vancouver

Hoshi N, Schenten D, Nish SA, Walther Z, Gagliani N, Flavell RA et al. MyD88 signalling in colonic mononuclear phagocytes drives colitis in IL-10-deficient mice. NAT COMMUN. 2012;3:1120. https://doi.org/10.1038/ncomms2113

Bibtex

@article{15e5b008406447f291b8f10e4f19e403,
title = "MyD88 signalling in colonic mononuclear phagocytes drives colitis in IL-10-deficient mice",
abstract = "Commensal bacterial sensing by Toll-like receptors is critical for maintaining intestinal homeostasis, but can lead to colitis in the absence of interleukin-10. Although Toll-like receptors are expressed in multiple cell types in the colon, the cell type(s) responsible for the development of colitis are currently unknown. Here we generated mice that are selectively deficient in MyD88 in various cellular compartments in an interleukin-10(-/-) setting. Although epithelial expression of MyD88 was dispensable, MyD88 expression in the mononuclear phagocyte compartment was required for colitis development. Specifically, phenotypically distinct populations of colonic mononuclear phagocytes expressed high levels of interleukin-1β, interleukin-23 and interleukin-6, and promoted T-helper 17 responses in the absence of interleukin-10. Thus, gut bacterial sensing through MyD88 in mononuclear phagocytes drives inflammatory bowel disease when unopposed by interleukin-10.",
keywords = "Animals, Colitis, Colon, Enzyme-Linked Immunosorbent Assay, Flow Cytometry, Interleukin-10, Interleukin-1beta, Interleukin-23, Interleukin-6, Mice, Myeloid Differentiation Factor 88, Phagocytes, Reverse Transcriptase Polymerase Chain Reaction, Signal Transduction, Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't",
author = "Namiko Hoshi and Dominik Schenten and Nish, {Simone A} and Zenta Walther and Nicola Gagliani and Flavell, {Richard A} and Boris Reizis and Zeli Shen and Fox, {James G} and Akiko Iwasaki and Ruslan Medzhitov",
year = "2012",
doi = "10.1038/ncomms2113",
language = "English",
volume = "3",
pages = "1120",
journal = "NAT COMMUN",
issn = "2041-1723",
publisher = "NATURE PUBLISHING GROUP",

}

RIS

TY - JOUR

T1 - MyD88 signalling in colonic mononuclear phagocytes drives colitis in IL-10-deficient mice

AU - Hoshi, Namiko

AU - Schenten, Dominik

AU - Nish, Simone A

AU - Walther, Zenta

AU - Gagliani, Nicola

AU - Flavell, Richard A

AU - Reizis, Boris

AU - Shen, Zeli

AU - Fox, James G

AU - Iwasaki, Akiko

AU - Medzhitov, Ruslan

PY - 2012

Y1 - 2012

N2 - Commensal bacterial sensing by Toll-like receptors is critical for maintaining intestinal homeostasis, but can lead to colitis in the absence of interleukin-10. Although Toll-like receptors are expressed in multiple cell types in the colon, the cell type(s) responsible for the development of colitis are currently unknown. Here we generated mice that are selectively deficient in MyD88 in various cellular compartments in an interleukin-10(-/-) setting. Although epithelial expression of MyD88 was dispensable, MyD88 expression in the mononuclear phagocyte compartment was required for colitis development. Specifically, phenotypically distinct populations of colonic mononuclear phagocytes expressed high levels of interleukin-1β, interleukin-23 and interleukin-6, and promoted T-helper 17 responses in the absence of interleukin-10. Thus, gut bacterial sensing through MyD88 in mononuclear phagocytes drives inflammatory bowel disease when unopposed by interleukin-10.

AB - Commensal bacterial sensing by Toll-like receptors is critical for maintaining intestinal homeostasis, but can lead to colitis in the absence of interleukin-10. Although Toll-like receptors are expressed in multiple cell types in the colon, the cell type(s) responsible for the development of colitis are currently unknown. Here we generated mice that are selectively deficient in MyD88 in various cellular compartments in an interleukin-10(-/-) setting. Although epithelial expression of MyD88 was dispensable, MyD88 expression in the mononuclear phagocyte compartment was required for colitis development. Specifically, phenotypically distinct populations of colonic mononuclear phagocytes expressed high levels of interleukin-1β, interleukin-23 and interleukin-6, and promoted T-helper 17 responses in the absence of interleukin-10. Thus, gut bacterial sensing through MyD88 in mononuclear phagocytes drives inflammatory bowel disease when unopposed by interleukin-10.

KW - Animals

KW - Colitis

KW - Colon

KW - Enzyme-Linked Immunosorbent Assay

KW - Flow Cytometry

KW - Interleukin-10

KW - Interleukin-1beta

KW - Interleukin-23

KW - Interleukin-6

KW - Mice

KW - Myeloid Differentiation Factor 88

KW - Phagocytes

KW - Reverse Transcriptase Polymerase Chain Reaction

KW - Signal Transduction

KW - Journal Article

KW - Research Support, N.I.H., Extramural

KW - Research Support, Non-U.S. Gov't

U2 - 10.1038/ncomms2113

DO - 10.1038/ncomms2113

M3 - SCORING: Journal article

C2 - 23047678

VL - 3

SP - 1120

JO - NAT COMMUN

JF - NAT COMMUN

SN - 2041-1723

ER -