title: Immunodominance of a single CTL epitope in a primate species with limited MHC class I polymorphism.
abstract: MHC class I molecules play a crucial role in immunity to viral infections by presenting viral peptides to cytotoxic T lymphocytes. One of the hallmarks of MHC class I genes in outbred populations is their extraordinary polymorphism, yet the significance of this diversity is poorly understood. Certain species with reduced MHC class I diversity, such as the cotton-top tamarin (Saguinus oedipus), are more susceptible to fatal viral infections. To explore the relationship between this primate's limited MHC class I diversity and its susceptibility to viruses, we infected five cotton-top tamarins with influenza virus. Every tamarin recognized the same immunodominant CTL epitope of the influenza nucleoprotein. Surprisingly, this nucleoprotein peptide was bound by Saoe-G*08, an MHC class I molecule expressed by every cotton-top tamarin. Two tamarins also made a subdominant response to an epitope of the matrix (M1) protein. This peptide appeared to be bound by another common MHC class I molecule. With the exception of an additional subdominant response to the polymerase (PB2) protein in one individual, no other influenza-specific CTL responses were detected. In populations or species with limited MHC class I polymorphism like the cotton-top tamarin, a dependence on shared MHC class I molecules may enhance susceptibility to viral infection, since viruses that evade MHC class I-restricted recognition in one individual will likely evade recognition in the majority of individuals.
authors.affiliation: Wisconsin Regional Primate Research Center, University of Wisconsin, Madison 53715, USA.
authors.forename: D T
authors.initials: DT
authors.lastname: Evans
authors.forename: M S
authors.initials: MS
authors.lastname: Piekarczyk
authors.forename: T M
authors.initials: TM
authors.lastname: Allen
authors.forename: J E
authors.initials: JE
authors.lastname: Boyson
authors.forename: M
authors.initials: M
authors.lastname: Yeager
authors.forename: A L
authors.initials: AL
authors.lastname: Hughes
authors.forename: F M
authors.initials: FM
authors.lastname: Gotch
authors.forename: V S
authors.initials: VS
authors.lastname: Hinshaw
authors.forename: D I
authors.initials: DI
authors.lastname: Watkins
mesh_terms: D000818:Animals; D017951:Antigen Presentation; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology; D002999:Clone Cells; D005805:Genes, MHC Class I / Q000276:immunology*; D015395:Histocompatibility Antigens Class I / Q000276:immunology; D016056:Immunodominant Epitopes / Q000276:immunology* / Q000378:metabolism; D009980:Influenza A virus / Q000276:immunology; D009698:Nucleoproteins / Q000276:immunology; D009976:Orthomyxoviridae Infections / Q000276:immunology; D011110:Polymorphism, Genetic / Q000276:immunology*; D012324:RNA-Dependent RNA Polymerase; D016865:Reassortant Viruses / Q000276:immunology; D012452:Saguinus; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology* / Q000378:metabolism; D014763:Viral Matrix Proteins / Q000276:immunology / Q000378:metabolism; D014764:Viral Proteins / Q000276:immunology
chemical_list: D015395:Histocompatibility Antigens Class I; D016056:Immunodominant Epitopes; C031540:M-protein, influenza virus; C488936:M1 protein, Influenza A virus; D009698:Nucleoproteins; C057027:PB2 protein, Influenzavirus A; D014763:Viral Matrix Proteins; D014764:Viral Proteins; D012324:RNA-Dependent RNA Polymerase