Determination of structural principles underlying three different modes of lymphocytic choriomeningitis virus escape from CTL recognition.

摘要: Lymphocytic choriomeningitis virus infection of H-2b mice generates a strong CD8+ CTL response mainly directed toward three immunodominant epitopes, one which, gp33, is presented by both H-2Db and H-2Kb MHC class I molecules. This acts as selective agent for the emergence viral escape variants. These variants generate altered peptide ligands (APLs) that, when molecules, antagonize recognition ultimately allow to evade cellular immune response. The APLs gp33 epitope particularly advantageous LCMV, it allows in context We have determined crystal structures different complex with H-2Kb. Comparison between these APL/MHC those index peptide/MHC reveals structural basis strategies used LCMV mutations: 1) conformational changes residues that are potential TCR contacts, 2) impairment APL binding cleft, 3) introduction subtle at TCR/pMHC interface, such removal single hydroxyl group.