{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Inclan-Rico JM"],"funding":["NIAID NIH HHS","U.S. Department of Health & Human Services | National Institutes of Health"],"pagination":["1181-1193"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9357342"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["21(10)"],"pubmed_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"],"journal":["Nature immunology"],"pubmed_title":["Basophils prime group 2 innate lymphoid cells for neuropeptide-mediated inhibition."],"pmcid":["PMC9357342"],"funding_grant_id":["RO1 AI131634","T32AI125185","T32 AI125185","3R01AI131634-02W1","R01 AI131634","R01 AI123224","RO1 AI123224"],"pubmed_authors":["Sy CB","Siracusa MC","Ponessa JJ","Beaulieu AM","Inclan-Rico JM","Lemenze AD","Valero-Pacheco N","Hernandez CM"],"additional_accession":[]},"is_claimable":false,"name":"Basophils prime group 2 innate lymphoid cells for neuropeptide-mediated inhibition.","description":"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","dates":{"release":"2020-01-01T00:00:00Z","publication":"2020 Oct","modification":"2025-04-18T15:25:06.961Z","creation":"2025-02-19T02:26:47.914Z"},"accession":"S-EPMC9357342","cross_references":{"pubmed":["32807943"],"doi":["10.1038/s41590-020-0753-y"]}}