Type 2 cytokine responses promote parasitic immunity and initiate tissue repair; however, they can also result in immunopathologies when not properly restricted. Although basophilia is recognized as a common feature of type 2 inflammation, the roles basophils play in regulating these responses are unknown. Here, we demonstrate that helminth-induced group 2 innate lymphoid cell (ILC2) responses are exaggerated in the absence of basophils, resulting in increased inflammation and diminished lung function. Additionally, we show that ILC2s from basophil-depleted mice express reduced amounts of the receptor for the neuropeptide neuromedin B (NMB). Critically, NMB stimulation inhibited ILC2 responses from control but not basophil-depleted mice, and basophils were sufficient to directly enhance NMB receptor expression on ILC2s. These studies suggest that basophils prime ILC2s to respond to neuron-derived signals necessary to maintain tissue integrity. Further, these data provide mechanistic insight into the functions of basophils and identify NMB as a potent inhibitor of type 2 inflammation.

2 型细胞因子反应促进寄生虫免疫并启动组织修复；然而，如果没有适当限制，它们也可能导致免疫病理学。尽管嗜碱性粒细胞被认为是 2 型炎症的共同特征，但嗜碱性粒细胞在调节这些反应中所起的作用尚不清楚。在这里，我们证明蠕虫诱导的第 2 组先天淋巴细胞 (ILC2) 反应在没有嗜碱性粒细胞的情况下被夸大，导致炎症增加和肺功能减弱。此外，我们发现来自嗜碱性粒细胞耗尽小鼠的 ILC2 表达的神经肽神经介质 B (NMB) 受体数量减少。至关重要的是，NMB 刺激抑制了对照而非嗜碱性粒细胞耗尽小鼠的 ILC2 反应，并且嗜碱性粒细胞足以直接增强 ILC2 上的 NMB 受体表达。这些研究表明，嗜碱性粒细胞启动 ILC2 以响应维持组织完整性所必需的神经元衍生信号。此外，这些数据提供了对嗜碱性粒细胞功能的机制洞察，并将 NMB 确定为 2 型炎症的有效抑制剂。