Journal
SCIENCE
Volume 356, Issue 6342, Pages 1076-1080Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aaj2067
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Funding
- Spanish Ministry of Science [FPU-AP2010-1524, Est13/00372]
- Institute of Health Carlos III (CIBERES)
- Wenner-Gren Foundation
- Spanish Ministry of Economy and Competitiveness [SAF2012-32728, SAF2015-65307-R]
- Institute of Health Carlos III [CIBERES-CB06/06/0002]
- Medical Research Council UK [MR/K01207X/1]
- Wellcome Centre for Cell-Matrix Research
- Medical Research Council [MR/M011755/1]
- European Union [CIG-631413]
- National Institutes of Health [HL068127, HL128746]
- German Research Council (DFG) [609/2-1]
- Wellcome Trust Intermediate Fellowship
- Wenner Gren Foundation Fellowship
- Medical Research Council [MR/M011755/1, MR/K01207X/2, MR/K01207X/1] Funding Source: researchfish
- Wellcome Trust [100171/Z/12/Z] Funding Source: researchfish
- MRC [MR/K01207X/2, MR/K01207X/1, MR/M011755/1] Funding Source: UKRI
- Wellcome Trust [100171/Z/12/Z] Funding Source: Wellcome Trust
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The type 2 immune response controls helminth infection and maintains tissue homeostasis but can lead to allergy and fibrosis if not adequately regulated. We have discovered local tissue-specific amplifiers of type 2-mediated macrophage activation. In the lung, surfactant protein A (SP-A) enhanced interleukin-4 (IL-4)-dependent macrophage proliferation and activation, accelerating parasite clearance and reducing pulmonary injury after infection with a lung-migrating helminth. In the peritoneal cavity and liver, C1q enhancement of type 2 macrophage activation was required for liver repair after bacterial infection, but resulted in fibrosis after peritoneal dialysis. IL-4 drives production of these structurally related defense collagens, SP-A and C1q, and the expression of their receptor, myosin 18A. These findings reveal the existence within different tissues of an amplification system needed for local type 2 responses.
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