{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Greco SH"],"funding":["S.H.G.","G.M.","NCI NIH HHS","U.S. National Institutes of Health"],"pagination":["185-94"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6608084"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["100(1)"],"pubmed_abstract":["Regulation of Toll-like receptor responses is critical for limiting tissue injury and autoimmunity in both sepsis and sterile inflammation. We found that Mincle, a C-type lectin receptor, regulates proinflammatory Toll-like receptor 4 signaling. Specifically, Mincle ligation diminishes Toll-like receptor 4-mediated inflammation, whereas Mincle deletion or knockdown results in marked hyperresponsiveness to lipopolysaccharide in vitro, as well as overwhelming lipopolysaccharide-mediated inflammation in vivo. Mechanistically, Mincle deletion does not up-regulate Toll-like receptor 4 expression or reduce interleukin 10 production after Toll-like receptor 4 ligation; however, Mincle deletion decreases production of the p38 mitogen-activated protein kinase-dependent inhibitory intermediate suppressor of cytokine signaling 1, A20, and ABIN3 and increases expression of the Toll-like receptor 4 coreceptor CD14. Blockade of CD14 mitigates the increased sensitivity of Mincle(-/-) leukocytes to Toll-like receptor 4 ligation. Collectively, we describe a major role for Mincle in suppressing Toll-like receptor 4 responses and implicate its importance in nonmycobacterial models of inflammation."],"journal":["Journal of leukocyte biology"],"pubmed_title":["Mincle suppresses Toll-like receptor 4 activation."],"pmcid":["PMC6608084"],"funding_grant_id":["R21 CA155649","CA168611","R01 CA168611","CA155649"],"pubmed_authors":["Ochi A","Miller G","Daley D","Mani VR","Pachter HL","Seifert L","Vahle AK","Barilla R","Batel J","Greco SH","Mahmood SK","Deutsch M","Hundeyin M","Torres-Hernandez A"],"additional_accession":[]},"is_claimable":false,"name":"Mincle suppresses Toll-like receptor 4 activation.","description":"Regulation of Toll-like receptor responses is critical for limiting tissue injury and autoimmunity in both sepsis and sterile inflammation. We found that Mincle, a C-type lectin receptor, regulates proinflammatory Toll-like receptor 4 signaling. Specifically, Mincle ligation diminishes Toll-like receptor 4-mediated inflammation, whereas Mincle deletion or knockdown results in marked hyperresponsiveness to lipopolysaccharide in vitro, as well as overwhelming lipopolysaccharide-mediated inflammation in vivo. Mechanistically, Mincle deletion does not up-regulate Toll-like receptor 4 expression or reduce interleukin 10 production after Toll-like receptor 4 ligation; however, Mincle deletion decreases production of the p38 mitogen-activated protein kinase-dependent inhibitory intermediate suppressor of cytokine signaling 1, A20, and ABIN3 and increases expression of the Toll-like receptor 4 coreceptor CD14. Blockade of CD14 mitigates the increased sensitivity of Mincle(-/-) leukocytes to Toll-like receptor 4 ligation. Collectively, we describe a major role for Mincle in suppressing Toll-like receptor 4 responses and implicate its importance in nonmycobacterial models of inflammation.","dates":{"release":"2016-01-01T00:00:00Z","publication":"2016 Jul","modification":"2025-04-22T20:35:10.261Z","creation":"2019-07-25T07:03:25Z"},"accession":"S-EPMC6608084","cross_references":{"pubmed":["26747838"],"doi":["10.1189/jlb.3a0515-185r","10.1189/jlb.3A0515-185R"]}}