Macrophage function in tissue repair and remodeling requires IL-4 or IL-13 with apoptotic cells
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 a...
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| Veröffentlicht in: | Science (American Association for the Advancement of Science) 2017-06, Vol.356 (6342), p.1072-1076 |
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| creator | 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 Gaglian, Nicola |
| description | 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. |
| doi_str_mv | 10.1126/science.aai8132 |
| format | Article |
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Grace ; Cabeza-Cabrerizo, Mar ; Tucci, Andrea ; Hughes, Lindsey D. ; Kong, Yong ; Weinstein, Jason S. ; Licona-Limon, Paula ; Schmid, Edward T. ; Pelorosso, Facundo ; Gaglian, Nicola</creator><creatorcontrib>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 ; Gaglian, Nicola</creatorcontrib><description>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. 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Grace</creatorcontrib><creatorcontrib>Cabeza-Cabrerizo, Mar</creatorcontrib><creatorcontrib>Tucci, Andrea</creatorcontrib><creatorcontrib>Hughes, Lindsey D.</creatorcontrib><creatorcontrib>Kong, Yong</creatorcontrib><creatorcontrib>Weinstein, Jason S.</creatorcontrib><creatorcontrib>Licona-Limon, Paula</creatorcontrib><creatorcontrib>Schmid, Edward T.</creatorcontrib><creatorcontrib>Pelorosso, Facundo</creatorcontrib><creatorcontrib>Gaglian, Nicola</creatorcontrib><title>Macrophage function in tissue repair and remodeling requires IL-4 or IL-13 with apoptotic cells</title><title>Science (American Association for the Advancement of Science)</title><addtitle>Science</addtitle><description>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. 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Grace ; Cabeza-Cabrerizo, Mar ; Tucci, Andrea ; Hughes, Lindsey D. ; Kong, Yong ; Weinstein, Jason S. ; Licona-Limon, Paula ; Schmid, Edward T. ; Pelorosso, Facundo ; Gaglian, Nicola</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c509t-f1ab48ccaf737ed3089483415909ddafdc2ff27910d49b1f1535f90eaf59f7743</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Ablation</topic><topic>Activation</topic><topic>Alveoli</topic><topic>Animal models</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Bacteria</topic><topic>Bacterial diseases</topic><topic>Cell activation</topic><topic>Cell adhesion</topic><topic>Cell proliferation</topic><topic>Chemotaxis</topic><topic>Colitis</topic><topic>Complement</topic><topic>Complement component C1q</topic><topic>Cytokines</topic><topic>Damage</topic><topic>Fibrosis</topic><topic>Gastrointestinal tract</topic><topic>Genes</topic><topic>Infections</topic><topic>Inflammation</topic><topic>Inflammation - chemically induced</topic><topic>Inflammation - pathology</topic><topic>Injuries</topic><topic>Injury prevention</topic><topic>Interleukin</topic><topic>Interleukin 13</topic><topic>Interleukin 4</topic><topic>Interleukin-13 - immunology</topic><topic>Interleukin-4 - immunology</topic><topic>Liver</topic><topic>Logical Thinking</topic><topic>Lungs</topic><topic>Macrophages</topic><topic>Macrophages - immunology</topic><topic>Mice</topic><topic>Nippostrongylus - physiology</topic><topic>Pattern recognition</topic><topic>Pattern recognition receptors</topic><topic>Peritoneum</topic><topic>Protein A</topic><topic>Regeneration</topic><topic>Repair</topic><topic>Rodents</topic><topic>Sensors</topic><topic>Strongylida Infections - immunology</topic><topic>Surfactant protein A</topic><topic>Thioglycolates</topic><topic>Tissue engineering</topic><topic>Tissues</topic><topic>Transcription</topic><topic>Wounding</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bosurgi, Lidia</creatorcontrib><creatorcontrib>Cao, Y. 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| ispartof | Science (American Association for the Advancement of Science), 2017-06, Vol.356 (6342), p.1072-1076 |
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| source | Jstor Complete Legacy; MEDLINE; Science Magazine |
| subjects | Ablation Activation Alveoli Animal models Animals Apoptosis Bacteria Bacterial diseases Cell activation Cell adhesion Cell proliferation Chemotaxis Colitis Complement Complement component C1q Cytokines Damage Fibrosis Gastrointestinal tract Genes Infections Inflammation Inflammation - chemically induced Inflammation - pathology Injuries Injury prevention Interleukin Interleukin 13 Interleukin 4 Interleukin-13 - immunology Interleukin-4 - immunology Liver Logical Thinking Lungs Macrophages Macrophages - immunology Mice Nippostrongylus - physiology Pattern recognition Pattern recognition receptors Peritoneum Protein A Regeneration Repair Rodents Sensors Strongylida Infections - immunology Surfactant protein A Thioglycolates Tissue engineering Tissues Transcription Wounding |
| title | Macrophage function in tissue repair and remodeling requires IL-4 or IL-13 with apoptotic cells |
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