PortalPublikationenMacrophage function in tissue repair and remodeling requires...

Macrophage function in tissue repair and remodeling requires IL-4 or IL-13 with apoptotic cells

Standard

Macrophage function in tissue repair and remodeling requires IL-4 or IL-13 with apoptotic cells. / Bosurgi, Lidia; Cao, Y Grace; Cabeza-Cabrerizo, Mar; Tucci, Andrea; Hughes, Lindsey D; Kong, Yong; Weinstein, Jason S; Licona-Limon, Paula; Schmid, Edward T; Pelorosso, Facundo; Gagliani, Nicola; Craft, Joseph E; Flavell, Richard A; Ghosh, Sourav; Rothlin, Carla V.

in: SCIENCE, Jahrgang 356, Nr. 6342, 09.06.2017, S. 1072-1076.

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

Harvard

Bosurgi, L, Cao, YG, Cabeza-Cabrerizo, M, Tucci, A, Hughes, LD, Kong, Y, Weinstein, JS, Licona-Limon, P, Schmid, ET, Pelorosso, F, Gagliani, N, Craft, JE, Flavell, RA, Ghosh, S & Rothlin, CV 2017, 'Macrophage function in tissue repair and remodeling requires IL-4 or IL-13 with apoptotic cells', SCIENCE, Jg. 356, Nr. 6342, S. 1072-1076. https://doi.org/10.1126/science.aai8132

APA

Bosurgi, L., Cao, Y. G., Cabeza-Cabrerizo, M., Tucci, A., Hughes, L. D., Kong, Y., Weinstein, J. S., Licona-Limon, P., Schmid, E. T., Pelorosso, F., Gagliani, N., Craft, J. E., Flavell, R. A., Ghosh, S., & Rothlin, C. V. (2017). Macrophage function in tissue repair and remodeling requires IL-4 or IL-13 with apoptotic cells. SCIENCE, 356(6342), 1072-1076. https://doi.org/10.1126/science.aai8132

Vancouver

Bosurgi L, Cao YG, Cabeza-Cabrerizo M, Tucci A, Hughes LD, Kong Y et al. Macrophage function in tissue repair and remodeling requires IL-4 or IL-13 with apoptotic cells. SCIENCE. 2017 Jun 9;356(6342):1072-1076. https://doi.org/10.1126/science.aai8132

Bibtex

@article{259d48d6f2d84a5e9534ab60407f6c0e,
title = "Macrophage function in tissue repair and remodeling requires IL-4 or IL-13 with apoptotic cells",
abstract = "Tissue repair is a subset of a broad repertoire of interleukin-4 (IL-4)- and IL-13-dependent host responses during helminth infection. Here we show that IL-4 or IL-13 alone was not sufficient, but IL-4 or IL-13 together with apoptotic cells induced the tissue repair program in macrophages. Genetic ablation of sensors of apoptotic cells impaired the proliferation of tissue-resident macrophages and the induction of anti-inflammatory and tissue repair genes in the lungs after helminth infection or in the gut after induction of colitis. By contrast, the recognition of apoptotic cells was dispensable for cytokine-dependent induction of pattern recognition receptor, cell adhesion, or chemotaxis genes in macrophages. Detection of apoptotic cells can therefore spatially compartmentalize or prevent premature or ectopic activity of pleiotropic, soluble cytokines such as IL-4 or IL-13.",
keywords = "Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural",
author = "Lidia Bosurgi and Cao, {Y Grace} and Mar Cabeza-Cabrerizo and Andrea Tucci and Hughes, {Lindsey D} and Yong Kong and Weinstein, {Jason S} and Paula Licona-Limon and Schmid, {Edward T} and Facundo Pelorosso and Nicola Gagliani and Craft, {Joseph E} and Flavell, {Richard A} and Sourav Ghosh and Rothlin, {Carla V}",
note = "Copyright {\textcopyright} 2017, American Association for the Advancement of Science.",
year = "2017",
month = jun,
day = "9",
doi = "10.1126/science.aai8132",
language = "English",
volume = "356",
pages = "1072--1076",
journal = "SCIENCE",
issn = "0036-8075",
publisher = "American Association for the Advancement of Science",
number = "6342",

}

RIS

TY - JOUR

T1 - Macrophage function in tissue repair and remodeling requires IL-4 or IL-13 with apoptotic cells

AU - Bosurgi, Lidia

AU - Cao, Y Grace

AU - Cabeza-Cabrerizo, Mar

AU - Tucci, Andrea

AU - Hughes, Lindsey D

AU - Kong, Yong

AU - Weinstein, Jason S

AU - Licona-Limon, Paula

AU - Schmid, Edward T

AU - Pelorosso, Facundo

AU - Gagliani, Nicola

AU - Craft, Joseph E

AU - Flavell, Richard A

AU - Ghosh, Sourav

AU - Rothlin, Carla V

N1 - Copyright © 2017, American Association for the Advancement of Science.

PY - 2017/6/9

Y1 - 2017/6/9

N2 - Tissue repair is a subset of a broad repertoire of interleukin-4 (IL-4)- and IL-13-dependent host responses during helminth infection. Here we show that IL-4 or IL-13 alone was not sufficient, but IL-4 or IL-13 together with apoptotic cells induced the tissue repair program in macrophages. Genetic ablation of sensors of apoptotic cells impaired the proliferation of tissue-resident macrophages and the induction of anti-inflammatory and tissue repair genes in the lungs after helminth infection or in the gut after induction of colitis. By contrast, the recognition of apoptotic cells was dispensable for cytokine-dependent induction of pattern recognition receptor, cell adhesion, or chemotaxis genes in macrophages. Detection of apoptotic cells can therefore spatially compartmentalize or prevent premature or ectopic activity of pleiotropic, soluble cytokines such as IL-4 or IL-13.

AB - Tissue repair is a subset of a broad repertoire of interleukin-4 (IL-4)- and IL-13-dependent host responses during helminth infection. Here we show that IL-4 or IL-13 alone was not sufficient, but IL-4 or IL-13 together with apoptotic cells induced the tissue repair program in macrophages. Genetic ablation of sensors of apoptotic cells impaired the proliferation of tissue-resident macrophages and the induction of anti-inflammatory and tissue repair genes in the lungs after helminth infection or in the gut after induction of colitis. By contrast, the recognition of apoptotic cells was dispensable for cytokine-dependent induction of pattern recognition receptor, cell adhesion, or chemotaxis genes in macrophages. Detection of apoptotic cells can therefore spatially compartmentalize or prevent premature or ectopic activity of pleiotropic, soluble cytokines such as IL-4 or IL-13.

KW - Journal Article

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

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

UR - http://www.scopus.com/inward/record.url?eid=2-s2.0-85019188120&partnerID=MN8TOARS

U2 - 10.1126/science.aai8132

DO - 10.1126/science.aai8132

M3 - SCORING: Journal article

C2 - 28495875

VL - 356

SP - 1072

EP - 1076

JO - SCIENCE

JF - SCIENCE

SN - 0036-8075

IS - 6342

ER -