{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Hussey K"],"funding":["Gerald Kerkut Charitable Trust","Morris Animal Foundation"],"pagination":["351"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8953681"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["11(3)"],"pubmed_abstract":["Devil facial tumour disease (DFTD) is a transmissible cancer that has circulated in the Tasmanian devil population for >25 years. Like other contagious cancers in dogs and devils, the way DFTD escapes the immune response of its host is a central question to understanding this disease. DFTD has a low major histocompatibility complex class I (MHC-I) expression due to epigenetic modifications, preventing host immune recognition of mismatched MHC-I molecules by T cells. However, the total MHC-I loss should result in natural killer (NK) cell activation due to the ‘missing self’. Here, we have investigated the expression of the nonclassical MHC-I, Saha-UD as a potential regulatory or suppressive mechanism for DFTD. A monoclonal antibody was generated against the devil Saha-UD that binds recombin"],"journal":["Pathogens (Basel, Switzerland)"],"pubmed_title":["Expression of the Nonclassical MHC Class I, Saha-UD in the Transmissible Cancer Devil Facial Tumour Disease (DFTD)."],"pmcid":["PMC8953681"],"funding_grant_id":["KA Hussey","D18ZO-104"],"pubmed_authors":["Siddle HV","Skjodt K","Pye R","Caldwell A","Hussey K","Kreiss A","Woods GM","Hamede R","Gastaldello A"],"additional_accession":[]},"is_claimable":false,"name":"Expression of the Nonclassical MHC Class I, Saha-UD in the Transmissible Cancer Devil Facial Tumour Disease (DFTD).","description":"Devil facial tumour disease (DFTD) is a transmissible cancer that has circulated in the Tasmanian devil population for >25 years. Like other contagious cancers in dogs and devils, the way DFTD escapes the immune response of its host is a central question to understanding this disease. DFTD has a low major histocompatibility complex class I (MHC-I) expression due to epigenetic modifications, preventing host immune recognition of mismatched MHC-I molecules by T cells. However, the total MHC-I loss should result in natural killer (NK) cell activation due to the ‘missing self’. Here, we have investigated the expression of the nonclassical MHC-I, Saha-UD as a potential regulatory or suppressive mechanism for DFTD. A monoclonal antibody was generated against the devil Saha-UD that binds recombin","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Mar","modification":"2026-04-08T17:36:20.179Z","creation":"2025-04-06T12:09:08.822Z"},"accession":"S-EPMC8953681","cross_references":{"pubmed":["35335675"],"doi":["10.3390/pathogens11030351"]}}