Evidence map›Paper›PMID 32404419›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2020

The molecular basis of how buried human leukocyte antigen polymorphism modulates natural killer cell function.

Philippa M Saunders, Bruce J MacLachlan, Phillip Pymm, Patricia T Illing, Yuanchen Deng, Shu Cheng Wong, Clare V L Oates, Anthony W Purcell, Jamie Rossjohn, Julian P Vivian and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.1field-weighted citation impact, top 22% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 26 citations in OpenAlex.

  1. 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 · 2026
    Article
  2. The Role of Killer Ig-like Receptors in Diseases from A to Z.International journal of molecular sciences · 2025
    Review
  3. Review
  4. Article
  5. Biology of HLA class I associated inflammatory diseases.Best practice & research. Clinical rheumatology · 2024
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Association of KIR Genes and MHC Class I Ligands with Atopic Dermatitis.Journal of immunology (Baltimore, Md. : 1950) · 2021
    Article
  11. Article
  12. Article
  13. Article
  14. High-Resolution Characterization ofFrontiers in immunology · 2021
    Article
  15. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 2 countries.

Philippa M SaundersDepartment of Microbiology and Immunology, Peter Doherty Institute for Infection and Immunity, The University of Melbourne, Melbourne, VIC 3010, Australia.
Bruce J MacLachlanInfection and Immunity Program, Biomedicine Discovery Institute, Monash University, Clayton, VIC 3800, Australia.ORCID 0000-0002-2685-2733
Phillip PymmInfection and Immunity Program, Biomedicine Discovery Institute, Monash University, Clayton, VIC 3800, Australia.
Patricia T IllingInfection and Immunity Program, Biomedicine Discovery Institute, Monash University, Clayton, VIC 3800, Australia.ORCID 0000-0002-3870-0796
Yuanchen DengDepartment of Microbiology and Immunology, Peter Doherty Institute for Infection and Immunity, The University of Melbourne, Melbourne, VIC 3010, Australia.
Shu Cheng WongDepartment of Microbiology and Immunology, Peter Doherty Institute for Infection and Immunity, The University of Melbourne, Melbourne, VIC 3010, Australia.
Clare V L OatesDepartment of Microbiology and Immunology, Peter Doherty Institute for Infection and Immunity, The University of Melbourne, Melbourne, VIC 3010, Australia.
Anthony W PurcellInfection and Immunity Program, Biomedicine Discovery Institute, Monash University, Clayton, VIC 3800, Australia.ORCID 0000-0003-0532-8331
Jamie RossjohnInfection and Immunity Program, Biomedicine Discovery Institute, Monash University, Clayton, VIC 3800, Australia; jamie.rossjohn@monash.edu julian.vivian@monash.edu agbrooks@unimelb.edu.au.ORCID 0000-0002-2020-7522
Julian P VivianInfection and Immunity Program, Biomedicine Discovery Institute, Monash University, Clayton, VIC 3800, Australia; jamie.rossjohn@monash.edu julian.vivian@monash.edu agbrooks@unimelb.edu.au.ORCID 0000-0002-9400-4437
Andrew G BrooksDepartment of Microbiology and Immunology, Peter Doherty Institute for Infection and Immunity, The University of Melbourne, Melbourne, VIC 3010, Australia; jamie.rossjohn@monash.edu julian.vivian@monash.edu agbrooks@unimelb.edu.au.ORCID 0000-0002-4085-9683
The University of Melbourne · AUAustralian Regenerative Medicine Institute · AUAustralian Research Council · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Micropolymorphisms within human leukocyte antigen (HLA) class I molecules can change the architecture of the peptide-binding cleft, leading to differences in peptide presentation and T cell recognition. The impact of such HLA variation on natural killer (NK) cell recognition remains unclear. Given the differential association of HLA-B*57:01 and HLA-B*57:03 with the control of HIV, recognition of these HLA-B57 allomorphs by the killer cell immunoglobulin-like receptor (KIR) 3DL1 was compared. Despite differing by only two polymorphic residues, both buried within the peptide-binding cleft, HLA-B*57:01 more potently inhibited NK cell activation. Direct-binding studies showed KIR3DL1 to preferentially recognize HLA-B*57:01, particularly when presenting peptides with positively charged position (P)Ω-2 residues. In HLA-B*57:01, charged PΩ-2 residues were oriented toward the peptide-binding cleft and away from KIR3DL1. In HLA-B*57:03, the charged PΩ-2 residues protruded out from the cleft and directly impacted KIR3DL1 engagement. Accordingly, KIR3DL1 recognition of HLA class I ligands is modulated by both the peptide sequence and conformation, as determined by the HLA polymorphic framework, providing a rationale for understanding differences in clinical associations.

Indexed as

Histocompatibility Antigens Class IHumansKiller Cells, NaturalLymphocyte ActivationModels, MolecularPolymorphism, GeneticReceptors, KIRHistocompatibility Antigens Class IReceptors, KIRHLAKIRnatural killer cells

Identifiers

PMID32404419
PMCPMC7261055
OpenAlexW3025170387

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.