期刊
NATURE IMMUNOLOGY
卷 21, 期 10, 页码 1181-+出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41590-020-0753-y
关键词
-
类别
资金
- National Institutes of Health [RO1 AI123224, RO1 AI131634, T32AI125185, 3R01AI131634-02W1]
- Mexican Council of Science Technology [CVU 536876]
Siracusa and colleagues reveal a regulatory role for basophils in the context of anti-helminth immunity and identify the neuropeptide neuromedin B as a potent inhibitor of type 2 inflammation. 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.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据