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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Immune selection for altered antigen processing leads to cytotoxic T lymphocyte escape in chronic HIV-1 infection.

Mutations within cytotoxic T lymphocyte (CTL) epitopes impair T cell recognition, but escape mutations arising in flanking regions that alter antigen processing have not been defined in natural human infections. In human histocompatibility leukocyte antigen (HLA)-B57+ HIV-infected persons, immune selection pressure leads to a mutation from alanine to proline at Gag residue 146 immediately preceding the NH2 terminus of a dominant HLA-B57-restricted epitope, ISPRTLNAW. Although N-extended wild-type or mutant peptides remained well-recognized, mutant virus-infected CD4 T cells failed to be recognized by the same CTL clones. The A146P mutation prevented NH2-terminal trimming of the optimal epitope by the endoplasmic reticulum aminopeptidase I. These results demonstrate that allele-associated sequence variation within the flanking region of CTL epitopes can alter antigen processing. Identifying such mutations is of major relevance in the construction of vaccine sequences.[1]

References

  1. Immune selection for altered antigen processing leads to cytotoxic T lymphocyte escape in chronic HIV-1 infection. Draenert, R., Le Gall, S., Pfafferott, K.J., Leslie, A.J., Chetty, P., Brander, C., Holmes, E.C., Chang, S.C., Feeney, M.E., Addo, M.M., Ruiz, L., Ramduth, D., Jeena, P., Altfeld, M., Thomas, S., Tang, Y., Verrill, C.L., Dixon, C., Prado, J.G., Kiepiela, P., Martinez-Picado, J., Walker, B.D., Goulder, P.J. J. Exp. Med. (2004) [Pubmed]
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