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 Just as infection needs to be limited, so must healing responses be contained to reduce scarring and allergy. 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.

中文翻译：

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组织修复和重塑中的巨噬细胞功能需要具有凋亡细胞的 IL-4 或 IL-13

局部巨噬细胞清理感染，尤其是蠕虫或细菌感染，可导致组织损伤（见 Bouchery 和 Harris 的观点）。米努蒂等人。研究了蠕虫感染和纤维化的小鼠模型。他们在肺中表达表面活性蛋白 A（补体成分 C1q 家族的成员），这增强了白细胞介素 4 (IL-4) 介导的肺泡巨噬细胞增殖和活化。这种激活加速了蠕虫清除并减少了肺损伤。在腹膜中，C1q 在细菌感染后促进巨噬细胞活化以进行肝脏修复。通过不同的方法，Bosurgi 等人。发现在肺部蠕虫迁移或小鼠肠道炎症期间造成伤害后，IL-4 和 IL-13 仅在凋亡细胞存在时起作用，以促进局部巨噬细胞的组织修复。科学，这个问题 1076 页。1072; 另见第。1014 正如需要限制感染一样，也必须控制愈合反应以减少疤痕和过敏。组织修复是蠕虫感染期间白细胞介素 4 (IL-4) 和 IL-13 依赖性宿主反应的一个子集。在这里，我们表明单独的 IL-4 或 IL-13 是不够的，但 IL-4 或 IL-13 与凋亡细胞一起诱导巨噬细胞中的组织修复程序。凋亡细胞传感器的基因消融会损害组织驻留巨噬细胞的增殖以及蠕虫感染后肺部或结肠炎诱导后肠道中抗炎和组织修复基因的诱导。相比之下，凋亡细胞的识别对于模式识别受体的细胞因子依赖性诱导、细胞粘附、或巨噬细胞中的趋化基因。因此，凋亡细胞的检测可以在空间上划分或防止多效性、可溶性细胞因子如 IL-4 或 IL-13 的过早或异位活性。