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

2017; American Association for the Advancement of Science; Volume: 356; Issue: 6342 Linguagem: Inglês

10.1126/science.aai8132

1095-9203

Lidia Bosurgi, Ying Cao, Mar Cabeza-Cabrerizo, A. Tucci, Lindsey D. Hughes, Yong Kong, Jason S. Weinstein, Paula Licona-Limón, Edward T. Schmid, Facundo Pelorosso, Nicola Gagliani, Joseph Craft, Richard A. Flavell, Sourav Ghosh, Carla V. Rothlin,

Neonatal Respiratory Health Research

Local macrophage clean-up Infection, especially by helminths or bacteria, can cause tissue damage (see the Perspective by Bouchery and Harris). Minutti et al. studied mouse models of helminth infection and fibrosis. They expressed surfactant protein A (a member of the complement component C1q family) in the lung, which enhanced interleukin-4 (IL-4)-mediated proliferation and activation of alveolar macrophages. This activation accelerated helminth clearance and reduced lung injury. In the peritoneum, C1q boosted macrophage activation for liver repair after bacterial infection. By a different approach, Bosurgi et al. discovered that after wounding caused by migrating helminths in the lung or during inflammation in the gut of mice, IL-4 and IL-13 act only in the presence of apoptotic cells to promote tissue repair by local macrophages. Science , this issue p. 1076 , p. 1072 ; see also p. 1014