Mutational Escape in HIV-1 CTL Epitopes Leads to Increased Binding to Inhibitory Myelomonocytic MHC Class I Receptors

Escape 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 C...

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Bibliographic Details
Main Authors: Yang, Yue (Contributor), Huang, Jinghe (Author), Toth, Ildiko (Author), Lichterfeld, Mathias (Author), Yu, Xu G. (Author)
Format: Article
Language:English
Published: Public Library of Science, 2011-07-20T21:05:06Z.
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Online Access:Get fulltext
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100 1 0 |a Yang, Yue  |e author 
100 1 0 |a Yang, Yue  |e contributor 
100 1 0 |a Yang, Yue  |e contributor 
700 1 0 |a Huang, Jinghe  |e author 
700 1 0 |a Toth, Ildiko  |e author 
700 1 0 |a Lichterfeld, Mathias  |e author 
700 1 0 |a Yu, Xu G.  |e author 
245 0 0 |a Mutational Escape in HIV-1 CTL Epitopes Leads to Increased Binding to Inhibitory Myelomonocytic MHC Class I Receptors 
260 |b Public Library of Science,   |c 2011-07-20T21:05:06Z. 
856 |z Get fulltext  |u http://hdl.handle.net/1721.1/64947 
520 |a Escape 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. 
520 |a National Institutes of Health (U.S.) (Grant R01 AI078799) 
520 |a National Institutes of Health (U.S.) (Grant P01 AI074415) 
520 |a Doris Duke Charitable Foundation 
546 |a en_US 
655 7 |a Article 
773 |t PLoS ONE