Protective effect of granular leukocytes on host defense against intestinal nematode infection

在这项研究中，我们证明了2组先天淋巴样细胞（ILC2s）在诱导肺嗜酸性粒细胞增多中的相关作用。委内瑞拉圆线虫（Strongyloides venezuela, Sv）感染通过增加II型肺泡上皮细胞的数量诱导IL-33的产生，这些细胞在其细胞核中表达IL-33。然后，IL-33诱导ILC2s增殖并产生IL-5和IL-13，两者共同诱导肺嗜酸性粒细胞炎症，帮助驱逐肺部感染的蠕虫。我们还发现，AID-/-小鼠在感染Sv后，缺乏从IgM转换到其他同种型的能力，通常会产生Th2细胞和肠肥大细胞增多症。然而，它们不能快速排出Sv，需要从感染Sv的小鼠中过继转移IgE和IgG才能获得迅速排出Sv的能力。因此，肠道线虫的快速排出需要先天免疫和获得性免疫。

In this study, we demonstrated the relevant roles of group 2 innate lymphoid cells (ILC2s) for induction of pulmonary eosinophilia. Infection with Strongyloides venezuelensis (Sv) induces IL-33 production by increasing the number of Type II alveolar epithelial cells, which express IL-33 in their nucleus. Then, IL-33 induces ILC2s to proliferate and produce IL-5 and IL-13, which in combination induce lung eosinophilic inflammation, aiding to expel infected worms in the lungs. We also showed that AID-/- mice, lacking the capacity to switch from IgM to other isotypes, normally develop Th2 cells and intestinal mastocytosis after infection with Sv.However, they failed to rapidly expel Sv and need adoptive transfers of IgE and IgG from Sv-infected mice to obtain the capacity to promptly expel Sv. Thus, both innate and acquired immunity are required for rapid expulsion of intestinal nematode.