Tissue-resident macrophages (TRMs) maintain tissue homeostasis, but they can also provide a replicative niche for intracellular pathogens such as Leishmania. How dermal TRMs proliferate and maintain their M2 properties even in the strong T_H1 environment of the L. major infected dermis is not clear. Here, we show that, in infected mice lacking IL-4/13 from eosinophils, dermal TRMs shifted to a proinflammatory state, their numbers declined, and disease was attenuated. Intravital microscopy revealed a rapid infiltration of eosinophils followed by their tight interaction with dermal TRMs. IL-4–stimulated dermal TRMs, in concert with IL-10, produced a large amount of CCL24, which functioned to amplify eosinophil influx and their interaction with dermal TRMs. An intraperitoneal helminth infection model also demonstrated a requirement for eosinophil-derived IL-4 to maintain tissue macrophages through a CCL24-mediated amplification loop. CCL24 secretion was confined to resident macrophages in other tissues, implicating eosinophil-TRM cooperative interactions in diverse inflammatory settings.

驻留在组织中的巨噬细胞（TRM）维持组织稳态，但是它们也可以为细胞内病原体（如利什曼原虫）提供复制性利基。如何真皮真有效值增殖和维护，即使在强T的M2性质_{^ h}的1环境硕大利什曼原虫感染的真皮尚不清楚。在这里，我们显示出，在嗜酸性粒细胞缺乏IL-4 / 13的感染小鼠中，皮肤TRM转变为促炎状态，其数量减少，疾病减轻。活体显微镜检查显示嗜酸性粒细胞迅速浸润，随后与皮肤TRM紧密相互作用。IL-4刺激的真皮TRM与IL-10共同产生了大量的CCL24，其作用是放大嗜酸性粒细胞流入及其与真皮TRM的相互作用。腹膜内蠕虫感染模型还证明了嗜酸性粒细胞来源的IL-4能够通过CCL24介导的扩增环维持组织巨噬细胞的需求。CCL24的分泌仅限于其他组织中的常驻巨噬细胞，这意味着在各种炎症环境中嗜酸性粒细胞-TRM合作相互作用。