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• W2042380240 endingPage "e1000186" @default.
• W2042380240 startingPage "e1000186" @default.
• W2042380240 abstract "High affinity antigen-specific T cells play a critical role during protective immune responses. Epitope enhancement can elicit more potent T cell responses and can subsequently lead to a stronger memory pool; however, the molecular basis of such enhancement is unclear. We used the consensus peptide-binding motif for the Major Histocompatibility Complex molecule H-2K(b) to design a heteroclitic version of the mouse hepatitis virus-specific subdominant S598 determinant. We demonstrate that a single amino acid substitution at a secondary anchor residue (Q to Y at position 3) increased the stability of the engineered determinant in complex with H-2K(b). The structural basis for this enhanced stability was associated with local alterations in the pMHC conformation as a result of the Q to Y substitution. Recombinant viruses encoding this engineered determinant primed CTL responses that also reacted to the wildtype epitope with significantly higher functional avidity, and protected against selection of virus mutated at a second CTL determinant and consequent disease progression in persistently infected mice. Collectively, our findings provide a basis for the enhanced immunogenicity of an engineered determinant that will serve as a template for guiding the development of heteroclitic T cell determinants with applications in prevention of CTL escape in chronic viral infections as well as in tumor immunity." @default.
• W2042380240 created "2016-06-24" @default.
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• W2042380240 date "2008-10-24" @default.
• W2042380240 modified "2023-09-27" @default.
• W2042380240 title "Prevention of Cytotoxic T Cell Escape Using a Heteroclitic Subdominant Viral T Cell Determinant" @default.
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• W2042380240 doi "https://doi.org/10.1371/journal.ppat.1000186" @default.
• W2042380240 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2563037" @default.
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• W2042380240 hasPublicationYear "2008" @default.
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