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 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.…

• NS
  National Science Foundation

  Awards: award305303, DGE-1122492
• HH
  Howard Hughes Medical Institute

  Award: award305304
• AC
  American-Italian Cancer Foundation

  Award: award305302
• NI
  National Institutes of Health

  Awards: award305300, award305299, R01CA212376, award305301, award309995, T32AI007019, R37 AR40072, R01 AI089824