Basophils prime group 2 innate lymphoid cells for neuropeptide-mediated inhibition.

ABSTRACT: 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 NM

SUBMITTER: Inclan-Rico JM 

PROVIDER: S-EPMC9357342 | biostudies-literature | 2020 Oct

REPOSITORIES: biostudies-literature