Group 2 innate lymphoid cells (ILC2s) possess indispensable roles during type 2–mediated inflammatory diseases. Although their physiological and detrimental immune functions seem to depend on the anatomical compartment they reside, their tissue tropism and the molecular and immunological processes regulating the self-renewal of the local pool of ILC2s in the context of inflammation or infection are incompletely understood. Here, we analyzed the role of the CC-chemokine receptor CCR8 for the biological functions of ILC2s. In vitro and in vivo experiments indicated that CCR8 is in comparison to the related molecule CCR4 less important for migration of these cells. However, we found that activated mouse and human ILC2s produce the CCR8 ligand CCL1 and are a major source of CCL1 in vivo. CCL1 signaling to ILC2s regulates their proliferation and supports their capacity to protect against helminthic infections. In summary, we identify a novel chemokine receptor–dependent mechanism by which ILC2s are regulated during type 2 responses.

第2组先天性淋巴样细胞（ILC2）在2型介导的炎症性疾病中起着不可或缺的作用。尽管它们的生理和有害免疫功能似乎取决于它们所处的解剖区室，但在炎症或感染的情况下，它们的组织嗜性以及调节ILC2s局部池自我更新的分子和免疫过程尚不完全清楚。在这里，我们分析了CC趋化因子受体CCR8对ILC2s生物学功能的作用。体外和体内实验表明，与相关分子CCR4相比，CCR8对这些细胞的迁移不太重要。但是，我们发现激活的小鼠和人类ILC2产生CCR8配体CCL1，并且是体内CCL1的主要来源。向ILC2s发出的CCL1信号调节其增殖并支持其抵御蠕虫感染的能力。总而言之，我们确定了一种新型的趋化因子受体依赖性机制，通过该机制可以在2型应答中调节ILC2s。