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