<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Greco SH</submitter><funding>NIDDK NIH HHS</funding><funding>NCI NIH HHS</funding><pagination>2816-27</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5026929</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>197(7)</volume><pubmed_abstract>Con A hepatitis is regarded as a T cell-mediated model of acute liver injury. Mincle is a C-type lectin receptor that is critical in the immune response to mycobacteria and fungi but does not have a well-defined role in preclinical models of non-pathogen-mediated inflammation. Because Mincle can ligate the cell death ligand SAP130, we postulated that Mincle signaling drives intrahepatic inflammation and liver injury in Con A hepatitis. Acute liver injury was assessed in the murine Con A hepatitis model using C57BL/6, Mincle(-/-), and Dectin-1(-/-) mice. The role of C/EBPβ and hypoxia-inducible factor-1α (HIF-1α) signaling was assessed using selective inhibitors. We found that Mincle was highly expressed in hepatic innate inflammatory cells and endothelial cells in both mice and humans. Fur</pubmed_abstract><journal>Journal of immunology (Baltimore, Md. : 1950)</journal><pubmed_title>Mincle Signaling Promotes Con A Hepatitis.</pubmed_title><pmcid>PMC5026929</pmcid><funding_grant_id>R01 CA168611</funding_grant_id><funding_grant_id>T32 CA193111</funding_grant_id><funding_grant_id>K08 DK085278</funding_grant_id><pubmed_authors>Katz SC</pubmed_authors><pubmed_authors>Nagaraj SV</pubmed_authors><pubmed_authors>Nikifrov Y</pubmed_authors><pubmed_authors>Whiteman C</pubmed_authors><pubmed_authors>Ochi A</pubmed_authors><pubmed_authors>Miller G</pubmed_authors><pubmed_authors>Kalabin A</pubmed_authors><pubmed_authors>Ravirala S</pubmed_authors><pubmed_authors>Daley D</pubmed_authors><pubmed_authors>Mani VR</pubmed_authors><pubmed_authors>Seifert L</pubmed_authors><pubmed_authors>Tejada K</pubmed_authors><pubmed_authors>Gutierrez J</pubmed_authors><pubmed_authors>Barilla R</pubmed_authors><pubmed_authors>Rokosh R</pubmed_authors><pubmed_authors>Salyana MA</pubmed_authors><pubmed_authors>Greco SH</pubmed_authors><pubmed_authors>Deutsch M</pubmed_authors><pubmed_authors>Hundeyin M</pubmed_authors><pubmed_authors>Gelb BE</pubmed_authors><pubmed_authors>Torres-Hernandez A</pubmed_authors></additional><is_claimable>false</is_claimable><name>Mincle Signaling Promotes Con A Hepatitis.</name><description>Con A hepatitis is regarded as a T cell-mediated model of acute liver injury. Mincle is a C-type lectin receptor that is critical in the immune response to mycobacteria and fungi but does not have a well-defined role in preclinical models of non-pathogen-mediated inflammation. Because Mincle can ligate the cell death ligand SAP130, we postulated that Mincle signaling drives intrahepatic inflammation and liver injury in Con A hepatitis. Acute liver injury was assessed in the murine Con A hepatitis model using C57BL/6, Mincle(-/-), and Dectin-1(-/-) mice. The role of C/EBPβ and hypoxia-inducible factor-1α (HIF-1α) signaling was assessed using selective inhibitors. We found that Mincle was highly expressed in hepatic innate inflammatory cells and endothelial cells in both mice and humans. Fur</description><dates><release>2016-01-01T00:00:00Z</release><publication>2016 Oct</publication><modification>2025-04-04T01:07:14.715Z</modification><creation>2019-03-27T02:24:31Z</creation></dates><accession>S-EPMC5026929</accession><cross_references><pubmed>27559045</pubmed><doi>10.4049/jimmunol.1600598</doi></cross_references></HashMap>