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|Title:||Mutational Escape in HIV-1 CTL Epitopes Leads to Increased Binding to Inhibitory Myelomonocytic MHC Class I Receptors|
|Authors:||Toth, Ildiko;Yang, Yue;Huang, Jinghe;Lichterfeld, Mathias;Yu, Xu|
|subject:||HIV;Biology;Anatomy and Physiology;immune physiology;immune cells;Biochemistry;Proteins;immune system proteins;major histocompatibility antigens;protein interactions;Immunology;antigen-presenting cells;T cells;Immunity;retrovirology and HIV immunopathogenesis;immune defense;immune deficiency;Microbiology;Virology;viral immune evasion;microbial mutation;Medicine;Clinical Immunology;Infectious Diseases;Viral Diseases|
|Publisher:||Public Library of Science|
|Description:||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.|
|Standard no:||Yang, Yue, Jinghe Huang, Ildiko Toth, Mathias Lichterfeld, and Xu G. Yu. 2010. Mutational escape in HIV-1 CTL epitopes leads to increased binding to inhibitory myelomonocytic MHC class I receptors. PLoS ONE 5(12): e15084.|
|Appears in Collections:||HMS Scholarly Articles|
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