ArticleNature structural & molecular biology2017
MHC-I peptides get out of the groove and enable a novel mechanism of HIV-1 escape.
Article in Nature structural & molecular biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
56 citing papers in PubMed.
- The Activation State of CD4 T Cells Alters Cellular Peptidase Activities, HIV Antigen Processing, and MHC Class I Presentation in a Sequence-Dependent Manner.Journal of immunology (Baltimore, Md. : 1950) · 2019Trial
- Oral Innate Immunity and the Role of Oral Epithelial Cells.Advances in experimental medicine and biology · 2026Review
- Profiling associations of interactive ligand-receptors (HLA class I and KIR gene products) with the progression to type 1 diabetes among seroconverted participants.Diabetologia · 2025Article
- Identification of T-Cell Epitopes and Vaccine Development for African Swine Fever Virus.Vaccines · 2025Review
- Developing T Cell Epitope-Based Vaccines Against Infection: Challenging but Worthwhile.Vaccines · 2025Review
- Inhibitory leukocyte immunoglobulin-like receptors, subfamily B (LILRBs) in human diseases: structure, roles, mechanisms, and clinical applications.Theranostics · 2025Review
- Crucial Parameters for Immunopeptidome Characterization: A Systematic Evaluation.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
- CD8Nature communications · 2024Article
- APE-Gen2.0: Expanding Rapid Class I Peptide-Major Histocompatibility Complex Modeling to Post-Translational Modifications and Noncanonical Peptide Geometries.Journal of chemical information and modeling · 2024Article
- MHC1/LILRB1 axis as an innate immune checkpoint for cancer therapy.Frontiers in immunology · 2024Review
- Bw4 ligand and direct T-cell receptor binding induced selection on HLA A and B alleles.Frontiers in immunology · 2023Article
- The structure of songbird MHC class I reveals antigen binding that is flexible at the N-terminus and static at the C-terminus.Frontiers in immunology · 2023Article
- Protective HLA-B57: T cell and natural killer cell recognition in HIV infection.Biochemical Society transactions · 2022Review
- T Cell Epitope Discovery in the Context of Distinct and Unique Indigenous HLA Profiles.Frontiers in immunology · 2022Review
- Unconventional modes of peptide-HLA-I presentation change the rules of TCR engagement.Discovery immunology · 2022Review
- Peptidomes and Structures Illustrate How SLA-I Micropolymorphism Influences the Preference of Binding Peptide Length.Frontiers in immunology · 2022Article
- Structures suggest an approach for converting weak self-peptide tumor antigens into superagonists for CD8 T cells in cancer.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- The role of micropeptides in biology.Cellular and molecular life sciences : CMLS · 2021Review
- Identification of Promiscuous African Swine Fever Virus T-Cell Determinants Using a Multiple Technical Approach.Vaccines · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
Abstract
Major histocompatibility complex class I (MHC-I) molecules play a crucial role in immunity by capturing peptides for presentation to T cells and natural killer (NK) cells. The peptide termini are tethered within the MHC-I antigen-binding groove, but it is unknown whether other presentation modes occur. Here we show that 20% of the HLA-B*57:01 peptide repertoire comprises N-terminally extended sets characterized by a common motif at position 1 (P1) to P2. Structures of HLA-B*57:01 presenting N-terminally extended peptides, including the immunodominant HIV-1 Gag epitope TW10 (TSTLQEQIGW), showed that the N terminus protrudes from the peptide-binding groove. The common escape mutant TSNLQEQIGW bound HLA-B*57:01 canonically, adopting a dramatically different conformation than the TW10 peptide. This affected recognition by killer cell immunoglobulin-like receptor (KIR) 3DL1 expressed on NK cells. We thus define a previously uncharacterized feature of the human leukocyte antigen class I (HLA-I) immunopeptidome that has implications for viral immune escape. We further suggest that recognition of the HLA-B*57:01-TW10 epitope is governed by a 'molecular tension' between the adaptive and innate immune systems.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.