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

在这项研究中，我们证明了第2组先天性淋巴样细胞（ILC 2）诱导肺嗜酸性粒细胞增多症的相关作用。委内瑞拉圆线虫（Sv）感染通过增加在其细胞核中表达IL-33的II型肺泡上皮细胞的数量来诱导IL-33的产生。然后，IL-33诱导ILC 2增殖并产生IL-5和IL-13，其组合诱导肺嗜酸性粒细胞炎症，帮助排出肺中受感染的蠕虫。我们还表明，AID-/-小鼠，缺乏从IgM抗体转换为其他同种型的能力，正常发展的Th 2细胞和肠道肥大细胞增多症后，感染Sv。然而，他们未能迅速驱逐Sv和需要过继转移的IgE和IgG从Sv感染的小鼠获得的能力，及时驱逐Sv。因此，先天性和获得性免疫都是快速驱逐肠道线虫所必需的。

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.