{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Liang S"],"funding":["NIAID NIH HHS"],"pagination":["8357-62"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC2448841"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["105(24)"],"pubmed_abstract":["The expression of Ig-like transcript (ILT) inhibitory receptors is a characteristic of tolerogenic dendritic cells (DCs). However, the mechanisms of modulation of DCs via ILT receptors remain poorly defined. HLA-G is a preferential ligand for several ILTs. Recently, we demonstrated that triggering of ILT4 by HLA-G1 inhibits maturation of human monocyte-derived conventional DCs and murine DCs from ILT4 transgenic mice, resulting in diminished expression of MHC class II molecules, CD80 and CD86 costimulatory molecules, and prolongation of skin allograft survival. Different isoforms of HLA-G have diverse effects on the efficiency to induce ILT-mediated signaling. In this work, we show that HLA-G1 tetrameric complex and HLA-G5 dimer, but not HLA-G5 monomer, induce strong ILT-mediated signaling"],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pubmed_title":["Modulation of dendritic cell differentiation by HLA-G and ILT4 requires the IL-6--STAT3 signaling pathway."],"pmcid":["PMC2448841"],"funding_grant_id":["R01 AI055923"],"pubmed_authors":["Liang S","Arase H","Horuzsko A","Ristich V","Carosella ED","Dausset J"],"additional_accession":[]},"is_claimable":false,"name":"Modulation of dendritic cell differentiation by HLA-G and ILT4 requires the IL-6--STAT3 signaling pathway.","description":"The expression of Ig-like transcript (ILT) inhibitory receptors is a characteristic of tolerogenic dendritic cells (DCs). However, the mechanisms of modulation of DCs via ILT receptors remain poorly defined. HLA-G is a preferential ligand for several ILTs. Recently, we demonstrated that triggering of ILT4 by HLA-G1 inhibits maturation of human monocyte-derived conventional DCs and murine DCs from ILT4 transgenic mice, resulting in diminished expression of MHC class II molecules, CD80 and CD86 costimulatory molecules, and prolongation of skin allograft survival. Different isoforms of HLA-G have diverse effects on the efficiency to induce ILT-mediated signaling. In this work, we show that HLA-G1 tetrameric complex and HLA-G5 dimer, but not HLA-G5 monomer, induce strong ILT-mediated signaling","dates":{"release":"2008-01-01T00:00:00Z","publication":"2008 Jun","modification":"2025-04-04T18:33:54.779Z","creation":"2019-03-27T00:15:46Z"},"accession":"S-EPMC2448841","cross_references":{"pubmed":["18550825"],"doi":["10.1073/pnas.0803341105"]}}