ILC2s and T cells cooperate to ensure maintenance of M2 macrophages for lung immunity against hookworms
ILC2s and T cells cooperate to ensure maintenance of M2 macrophages for lung immunity against hookworms
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DOI：
10.1038/ncomms7970
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发表时间：
2015-04-01
影响因子：
16.6
通讯作者：
Le Gros, Graham
中科院分区：
文献类型：
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作者：
Bouchery, Tiffany;Kyle, Ryan;Le Gros, Graham
确定保护性免疫蠕虫感染的免疫机制仍然是一个重要的挑战。在这里，我们报告肺CD 4（+）T细胞和第2组先天淋巴细胞（ILC 2）协同工作，以阻止日本圆线虫（Nb）的发展在实质内的48小时内在小鼠。免疫损伤的幼虫具有显著的形态缺陷，其依赖于产生IL-13的ILC 2和CD 4（+）T细胞的扩增以及M2巨噬细胞的活化。这种T细胞需求可以通过施用IL-2或IL-33来绕过，导致产生IL-13的ILC 2的扩增和幼虫杀死。ILC 2的耗尽抑制IL-2处理的小鼠中的幼虫杀死。我们的研究结果拓宽了对ILC 2在蠕虫免疫中的作用的理解，证明它们不仅作为警报传感器，而且还可以由CD 4（+）T细胞维持，确保肺中IL-13依赖性M2巨噬细胞免疫的迅速激活和维持。
Defining the immune mechanisms underlying protective immunity to helminth infection remains an important challenge. Here we report that lung CD4(+) T cells and Group 2 innate lymphoid cells (ILC2s) work in concert to block Nippostrongylus brasiliensis (Nb) development in the parenchyma within 48 h in mice. Immune-damaged larvae have a striking morphological defect that is dependent on the expansion of IL-13-producing ILC2 and CD4(+) T cells, and the activation of M2 macrophages. This T-cell requirement can be bypassed by administration of IL-2 or IL-33, resulting in expansion of IL-13-producing ILC2s and larval killing. Depletion of ILC2s inhibits larval killing in IL-2-treated mice. Our results broaden understanding of ILC2's role in immunity to helminths by demonstrating that they not only act as alarmin sensors, but can also be sustained by CD4(+) T cells, ensuring both the prompt activation and the maintenance of IL-13-dependent M2 macrophage immunity in the lung.