{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Schick J"],"funding":["Deutsche Forschungsgemeinschaft"],"pagination":["e72923"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9908076"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["12"],"pubmed_abstract":["The myeloid C-type lectin receptor (CLR) MINCLE senses the mycobacterial cell wall component trehalose-6,6'-dimycolate (TDM). Recently, we found that IL-4 downregulates MINCLE expression in macrophages. IL-4 is a hallmark cytokine in helminth infections, which appear to increase the risk for mycobacterial infection and active tuberculosis. Here, we investigated functional consequences of IL-4 and helminth infection on MINCLE-driven macrophage activation and Th1/Th17 adjuvanticity. IL-4 inhibited MINCLE and cytokine induction after macrophage infection with <i>Mycobacterium bovis</i> bacille Calmette-Guerin (BCG). Infection of mice with BCG upregulated MINCLE on myeloid cells, which was inhibited by IL-4 plasmid injection and by infection with the nematode <i>Nippostrongylus brasiliensis</i"],"journal":["eLife"],"pubmed_title":["IL-4 and helminth infection downregulate MINCLE-dependent macrophage response to mycobacteria and Th17 adjuvanticity."],"pmcid":["PMC9908076"],"funding_grant_id":["LA 1262/8-1","CO 1469/16-1","CDC 1181_A02"],"pubmed_authors":["Schubart C","Westermann S","Lacorcia M","Bodendorfer B","Altunay M","Marschner N","Alexander C","da Costa CP","Lang R","Schick J","Christensen D","Schluckebier J","Wirtz S","Voehringer D"],"additional_accession":[]},"is_claimable":false,"name":"IL-4 and helminth infection downregulate MINCLE-dependent macrophage response to mycobacteria and Th17 adjuvanticity.","description":"The myeloid C-type lectin receptor (CLR) MINCLE senses the mycobacterial cell wall component trehalose-6,6'-dimycolate (TDM). Recently, we found that IL-4 downregulates MINCLE expression in macrophages. IL-4 is a hallmark cytokine in helminth infections, which appear to increase the risk for mycobacterial infection and active tuberculosis. Here, we investigated functional consequences of IL-4 and helminth infection on MINCLE-driven macrophage activation and Th1/Th17 adjuvanticity. IL-4 inhibited MINCLE and cytokine induction after macrophage infection with <i>Mycobacterium bovis</i> bacille Calmette-Guerin (BCG). Infection of mice with BCG upregulated MINCLE on myeloid cells, which was inhibited by IL-4 plasmid injection and by infection with the nematode <i>Nippostrongylus brasiliensis</i","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Feb","modification":"2025-04-04T18:43:32.965Z","creation":"2025-04-04T18:43:32.965Z"},"accession":"S-EPMC9908076","cross_references":{"pubmed":["36753434"],"doi":["10.7554/eLife.72923"]}}