4G8I
Crystal Structure of HLA B2705-KK10-L6M
Summary for 4G8I
Entry DOI | 10.2210/pdb4g8i/pdb |
Related | 4G8E 4G8F 4G8G 4G9D 4G9F |
Descriptor | HLA class I histocompatibility antigen, B-27 alpha chain, Beta-2-microglobulin, Gag protein, ... (5 entities in total) |
Functional Keywords | tcr, t cell, hla b*2705, kk10, kk10-l6m, hiv, immune escape, immune system |
Biological source | Homo sapiens (human) More |
Cellular location | Membrane; Single-pass type I membrane protein: P03989 Secreted . Note=(Microbial infection) In the presence of M: P61769 |
Total number of polymer chains | 3 |
Total formula weight | 45060.06 |
Authors | Gras, S.,Wilmann, P.G.,Rossjohn, J. (deposition date: 2012-07-23, release date: 2013-03-20, Last modification date: 2023-09-13) |
Primary citation | Ladell, K.,Hashimoto, M.,Iglesias, M.C.,Wilmann, P.G.,McLaren, J.E.,Gras, S.,Chikata, T.,Kuse, N.,Fastenackels, S.,Gostick, E.,Bridgeman, J.S.,Venturi, V.,Arkoub, Z.A.,Agut, H.,van Bockel, D.J.,Almeida, J.R.,Douek, D.C.,Meyer, L.,Venet, A.,Takiguchi, M.,Rossjohn, J.,Price, D.A.,Appay, V. A Molecular Basis for the Control of Preimmune Escape Variants by HIV-Specific CD8(+) T Cells. Immunity, 38:425-436, 2013 Cited by PubMed Abstract: The capacity of the immune system to adapt to rapidly evolving viruses is a primary feature of effective immunity, yet its molecular basis is unclear. Here, we investigated protective HIV-1-specific CD8+ T cell responses directed against the immunodominant p24 Gag-derived epitope KK10 (KRWIILGLNK263-272) presented by human leukocyte antigen (HLA)-B∗2705. We found that cross-reactive CD8+ T cell clonotypes were mobilized to counter the rapid emergence of HIV-1 variants that can directly affect T cell receptor (TCR) recognition. These newly recruited clonotypes expressed TCRs that engaged wild-type and mutant KK10 antigens with similar affinities and almost identical docking modes, thereby accounting for their antiviral efficacy in HLA-B∗2705+ individuals. A protective CD8+ T cell repertoire therefore encompasses the capacity to control TCR-accessible mutations, ultimately driving the development of more complex viral escape variants that disrupt antigen presentation. PubMed: 23521884DOI: 10.1016/j.immuni.2012.11.021 PDB entries with the same primary citation |
Experimental method | X-RAY DIFFRACTION (1.6 Å) |
Structure validation
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