Enables beta-2-microglobulin binding activity and peptide binding activity. Involved in T cell tolerance induction; negative regulation of natural killer cell mediated cytotoxicity; and positive regulation of adaptive immune response based on somatic recombination of immune receptors built from immunoglobulin superfamily domains. Predicted to be located in lumenal side of endoplasmic reticulum membrane and phagocytic vesicle membrane. Predicted to be part of MHC class I protein complex. Predicted to be active in external side of plasma membrane and extracellular space. Used to study graft-versus-host disease. Human ortholog(s) of this gene implicated in several diseases, including artery disease (multiple); asthma (multiple); autoimmune disease (multiple); eye disease (multiple); and inner ear disease (multiple). Orthologous to several human genes including HLA-B (major histocompatibility complex, class I, B); HLA-C (major histocompatibility complex, class I, C); and HLA-E (major histocompatibility complex, class I, E); PARTICIPATES IN allograft rejection pathway; antigen processing and presentation pathway; autoimmune thyroiditis pathway; INTERACTS WITH 2,3,7,8-tetrachlorodibenzodioxine; acetamide; ammonium acetate.
RT1 class I gene (A-1); RT1 class Ia, A1n; RT1 class Ia, locus A (A1); RT1 class Ia, locus A1 (mapped); RT1-A; RT1-A1_mapped; RT1-A1n; RT1.A1(N); RT1A-1
Donor-derived soluble MHC antigens plus low-dose cyclosporine induce transplantation unresponsiveness independent of the thymus by down-regulating T cell-mediated alloresponses in a rat transplantation model.
Oral feeding of an immunodominant MHC donor-derived synthetic class I peptide prolongs graft survival of heterotopic cardiac allografts in a high-responder rat strain combination.