AI Article Synopsis
- Tissue repair during helminth infections relies on both IL-4 or IL-13 and the presence of apoptotic cells to activate macrophages.
- Genetic removal of apoptotic cell sensors hinders the ability of tissue-resident macrophages to proliferate and promote anti-inflammatory responses in the lungs and gut.
- Recognizing apoptotic cells helps to manage the effects of cytokines like IL-4 and IL-13, ensuring they are activated appropriately without causing unwanted responses.
Article 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.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5556699 | PMC |
| http://dx.doi.org/10.1126/science.aai8132 | DOI Listing |
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