{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Umeshappa CS"],"funding":["Canadian Institutes of Health Research","CIHR"],"pagination":["1823-1829"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7108901"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["130(4)"],"pubmed_abstract":["Peptide MHC class II-based (pMHCII-based) nanomedicines trigger the formation of multicellular regulatory networks by reprogramming autoantigen-experienced CD4+ T cells into autoimmune disease-suppressing T regulatory type 1 (TR1) cells. We have shown that pMHCII-based nanomedicines displaying liver autoimmune disease-relevant yet ubiquitously expressed antigens can blunt various liver autoimmune disorders in a non-disease-specific manner without suppressing local or systemic immunity against infectious agents or cancer. Here, we show that such ubiquitous autoantigen-specific T cells are also awakened by extrahepatic tissue damage and that the corresponding TR1 progeny can suppress experimental autoimmune encephalomyelitis (EAE) and pancreatic β cell autoreactivity. In mice having EAE, nan"],"journal":["The Journal of clinical investigation"],"pubmed_title":["Ubiquitous antigen-specific T regulatory type 1 cells variably suppress hepatic and extrahepatic autoimmunity."],"pmcid":["PMC7108901"],"funding_grant_id":["FRN 136866"],"pubmed_authors":["Umeshappa CS","Santamaria P","Mohapatra S","Christen U","Yang Y","Ellestad KK","Lee JA","Shao K","Singha S","Nanjundappa RH","Yamanouchi J","Mbongue J"],"additional_accession":[]},"is_claimable":false,"name":"Ubiquitous antigen-specific T regulatory type 1 cells variably suppress hepatic and extrahepatic autoimmunity.","description":"Peptide MHC class II-based (pMHCII-based) nanomedicines trigger the formation of multicellular regulatory networks by reprogramming autoantigen-experienced CD4+ T cells into autoimmune disease-suppressing T regulatory type 1 (TR1) cells. We have shown that pMHCII-based nanomedicines displaying liver autoimmune disease-relevant yet ubiquitously expressed antigens can blunt various liver autoimmune disorders in a non-disease-specific manner without suppressing local or systemic immunity against infectious agents or cancer. Here, we show that such ubiquitous autoantigen-specific T cells are also awakened by extrahepatic tissue damage and that the corresponding TR1 progeny can suppress experimental autoimmune encephalomyelitis (EAE) and pancreatic β cell autoreactivity. In mice having EAE, nan","dates":{"release":"2020-01-01T00:00:00Z","publication":"2020 Apr","modification":"2025-04-04T22:00:41.016Z","creation":"2025-04-04T22:00:41.016Z"},"accession":"S-EPMC7108901","cross_references":{"pubmed":["32125290"],"doi":["10.1172/jci130670","10.1172/JCI130670"]}}