Linked Life Data

21170342

Source:http://linkedlifedata.com/resource/pubmed/id/21170342

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pubmed-article:21170342pubmed:abstractTextEscape mutations in HIV-1 cytotoxic T cell (CTL) epitopes can abrogate recognition by the TCR of HIV-1-specific CD8+ T cells, but may also change interactions with alternative MHC class I receptors. Here, we show that mutational escape in three HLA-A11-, B8- and B7- restricted immunodominant HIV-1 CTL epitopes consistently enhances binding of the respective peptide/MHC class I complex to Immunoglobulin-like transcript 4 (ILT4), an inhibitory myelomonocytic MHC class I receptor expressed on monocytes and dendritic cells. In contrast, mutational escape in an alternative immunodominant HLA-B57-restricted CTL epitope did not affect ILT4-mediated recognition by myelomonocytic cells. This suggests that in addition to abrogating recognition by HIV-1-specific CD8 T cells, mutational escape in some, but not all CTL epitopes may mediate important immunoregulatory effects by increasing binding properties to ILT4, and augmenting ILT4-mediated inhibitory effects of professional antigen-presenting cells.lld:pubmed
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pubmed-article:21170342pubmed:authorpubmed-author:LichterfeldMa...lld:pubmed
pubmed-article:21170342pubmed:authorpubmed-author:YuXu GXGlld:pubmed
pubmed-article:21170342pubmed:authorpubmed-author:YangYueYlld:pubmed
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pubmed-article:21170342pubmed:authorpubmed-author:HuangJingheJlld:pubmed
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pubmed-article:21170342pubmed:dateRevised2011-11-17lld:pubmed
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pubmed-article:21170342pubmed:year2010lld:pubmed
pubmed-article:21170342pubmed:articleTitleMutational escape in HIV-1 CTL epitopes leads to increased binding to inhibitory myelomonocytic MHC class I receptors.lld:pubmed
pubmed-article:21170342pubmed:affiliationRagon Institute of Massachusetts General Hospital, Harvard and MIT, Boston, Massachusetts, United States of America. xyu@partners.orglld:pubmed
pubmed-article:21170342pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:21170342pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
pubmed-article:21170342pubmed:publicationTypeResearch Support, N.I.H., Extramurallld:pubmed