ArticleNature communications2023
Molecular basis of differential HLA class I-restricted T cell recognition of a highly networked HIV peptide.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 29 citations in OpenAlex.
- Co-regulation of HIV control and cytomegalovirus pp65-specific IL-1β and TNF-α responses by genetic variants in the MHC region.PLoS pathogens · 2026Article
- HLA micropolymorphisms confine neoantigen conformational adaptability and guide T cell receptor selectivity.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Duration of Initial Viremia Modulates Functional Properties of HIV-specific T Cell Receptors.Research square · 2026Article
- Duration of Initial Viremia Modulates Functional Properties of HIV-specific T Cell Receptors.bioRxiv : the preprint server for biology · 2026Article
- Article
- A functionally validated TCR-pMHC database for TCR specificity model development.bioRxiv : the preprint server for biology · 2025Article
- TCR catch bonds nonlinearly control CD8 cooperation to shape T cell specificity.Cell research · 2025Article
- Dynamic allostery in the peptide/MHC complex enables TCR neoantigen selectivity.Nature communications · 2025Article
- Identification of a Clade-Specific HLA-C*03:02 CTL Epitope GY9 Derived from the HIV-1 p17 Matrix Protein.International journal of molecular sciences · 2024Article
- Polymorphic residues in HLA-B that mediate HIV control distinctly modulate peptide interactions with both TCR and KIR molecules.Structure (London, England : 1993) · 2024Article
- Multi-epitope peptide vaccines targeting dengue virus serotype 2 created via immunoinformatic analysis.Scientific reports · 2024Article
- Dynamic allostery in the peptide/MHC complex enables TCR neoantigen selectivity.Research square · 2024Article
- Commensal bacteria maintain a Qa-1eLife · 2023Article
Corrections and comments
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Authors and funding
21 authors at 6 institutions in 2 countries.
Funding
Abstract
Cytotoxic-T-lymphocyte (CTL) mediated control of HIV-1 is enhanced by targeting highly networked epitopes in complex with human-leukocyte-antigen-class-I (HLA-I). However, the extent to which the presenting HLA allele contributes to this process is unknown. Here we examine the CTL response to QW9, a highly networked epitope presented by the disease-protective HLA-B57 and disease-neutral HLA-B53. Despite robust targeting of QW9 in persons expressing either allele, T cell receptor (TCR) cross-recognition of the naturally occurring variant QW9_S3T is consistently reduced when presented by HLA-B53 but not by HLA-B57. Crystal structures show substantial conformational changes from QW9-HLA to QW9_S3T-HLA by both alleles. The TCR-QW9-B53 ternary complex structure manifests how the QW9-B53 can elicit effective CTLs and suggests sterically hindered cross-recognition by QW9_S3T-B53. We observe populations of cross-reactive TCRs for B57, but not B53 and also find greater peptide-HLA stability for B57 in comparison to B53. These data demonstrate differential impacts of HLAs on TCR cross-recognition and antigen presentation of a naturally arising variant, with important implications for vaccine design.
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