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Mutational Escape in HIV-1 CTL Epitopes Leads to Increased Binding to Inhibitory Myelomonocytic MHC Class I Receptors (HIV-1 CTL Escape Mutations and ILT4)

Yang, Yue ; Huang, Jinghe ; Toth, Ildiko ; Lichterfeld, Mathias ; Yu, Xu G; Poh, Lisa Ng Fong (Editor)

PLoS ONE, 2010, Vol.5(12), p.e15084 [Tạp chí có phản biện]

E-ISSN: 1932-6203 ; DOI: 10.1371/journal.pone.0015084

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  • Nhan đề:
    Mutational Escape in HIV-1 CTL Epitopes Leads to Increased Binding to Inhibitory Myelomonocytic MHC Class I Receptors (HIV-1 CTL Escape Mutations and ILT4)
  • Tác giả: Yang, Yue ; Huang, Jinghe ; Toth, Ildiko ; Lichterfeld, Mathias ; Yu, Xu G
  • Poh, Lisa Ng Fong (Editor)
  • Chủ đề: Research Article ; Biology ; Medicine ; Immunology ; Virology ; Infectious Diseases ; Microbiology ; Physiology ; Biochemistry
  • Là 1 phần của: PLoS ONE, 2010, Vol.5(12), p.e15084
  • Mô tả: 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.
  • Ngôn ngữ: English
  • Số nhận dạng: E-ISSN: 1932-6203 ; DOI: 10.1371/journal.pone.0015084

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