dc.contributor.author | Yang, Yue | |
dc.contributor.author | Huang, Jinghe | |
dc.contributor.author | Toth, Ildiko | |
dc.contributor.author | Lichterfeld, Mathias | |
dc.contributor.author | Yu, Xu G. | |
dc.date.accessioned | 2011-07-20T21:05:06Z | |
dc.date.available | 2011-07-20T21:05:06Z | |
dc.date.issued | 2010-12 | |
dc.date.submitted | 2010-08 | |
dc.identifier.issn | 1932-6203 | |
dc.identifier.uri | http://hdl.handle.net/1721.1/64947 | |
dc.description.abstract | 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. | en_US |
dc.description.sponsorship | National Institutes of Health (U.S.) (Grant R01 AI078799) | en_US |
dc.description.sponsorship | National Institutes of Health (U.S.) (Grant P01 AI074415) | en_US |
dc.description.sponsorship | Doris Duke Charitable Foundation | en_US |
dc.language.iso | en_US | |
dc.publisher | Public Library of Science | en_US |
dc.relation.isversionof | http://dx.doi.org/10.1371/journal.pone.0015084 | en_US |
dc.rights | Creative Commons Attribution | en_US |
dc.rights.uri | http://creativecommons.org/licenses/by/2.5/ | en_US |
dc.source | PLoS | en_US |
dc.title | Mutational Escape in HIV-1 CTL Epitopes Leads to Increased Binding to Inhibitory Myelomonocytic MHC Class I Receptors | en_US |
dc.type | Article | en_US |
dc.identifier.citation | Yang, Yue, Huang J, Toth I, Lichterfeld M, Yu XG (2010) Mutational Escape in HIV-1 CTL Epitopes Leads to Increased Binding to Inhibitory Myelomonocytic MHC Class I Receptors. PLoS ONE 5(12): e15084. © 2010 Yang et al. | en_US |
dc.contributor.approver | Yang, Yue | |
dc.contributor.mitauthor | Yang, Yue | |
dc.relation.journal | PLoS ONE | en_US |
dc.eprint.version | Final published version | en_US |
dc.type.uri | http://purl.org/eprint/type/JournalArticle | en_US |
eprint.status | http://purl.org/eprint/status/PeerReviewed | en_US |
dspace.orderedauthors | Yang, Yue; Huang, Jinghe; Toth, Ildiko; Lichterfeld, Mathias; Yu, Xu G. | en |
mit.license | PUBLISHER_CC | en_US |
mit.metadata.status | Complete | |