Evidence map›Paper›PMID 28695291›Full record

ReviewImmunogenetics2017

Missing or altered self: human NK cell receptors that recognize HLA-C.

Hugo G Hilton, Peter Parham

Open access · greenAbstract readReview
In one paragraph

Review in Immunogenetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

63 citing papers in PubMed, 83 citations in OpenAlex.

  1. Trial
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  11. DonorFrontiers in immunology · 2024
    Article
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  20. Prednisolone and enoxaparin (clexane) therapy ('the Bondi protocol') for repeated IVF failure.American journal of reproductive immunology (New York, N.Y. : 1989) · 2022
    Article

3 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Hugo G HiltonDepartments of Structural Biology and Microbiology & Immunology, Stanford University, Fairchild D-159, 299 Campus Drive West, Stanford, CA, 94305, USA.
Peter ParhamDepartments of Structural Biology and Microbiology & Immunology, Stanford University, Fairchild D-159, 299 Campus Drive West, Stanford, CA, 94305, USA. peropa@stanford.edu.
Fairchild Semiconductor (United States) · US

Funding

STRUCTURAL BIOLOGY OF HLA-A,B ANTIGENSR01AI017892 · NIAID · STANFORD UNIVERSITY · PI PARHAM, PETER R · 1985 to 2019
$6.1M
INTERACTIONS BETWEEN HLA CLASS I &CYTOLYTIC LYMPHOCYTESR01AI022039 · NIAID · STANFORD UNIVERSITY · PI PARHAM, PETER R · 1985 to 2017
$5.2M
NIAID NIH HHS R01 AI017892NIAID NIH HHS R01 AI022039
6 · The paper itself

Abstract

Natural killer (NK) cells are fast-acting and versatile lymphocytes that are critical effectors of innate immunity, adaptive immunity, and placental development. Controlling NK cell function are the interactions between killer-cell immunoglobulin-like receptors (KIRs) and their HLA-A, HLA-B and HLA-C ligands. Due to the extensive polymorphism of both KIR and HLA class I, these interactions are highly diversified and specific combinations correlate with protection or susceptibility to a range of infectious, autoimmune, and reproductive disorders. Evolutionary, genetic, and functional studies are consistent with the interactions between KIR and HLA-C being the dominant control mechanism of human NK cells. In addition to their recognition of the C1 and C2 epitopes, increasing evidence points to KIR having a previously unrecognized selectivity for the peptide presented by HLA-C. This selectivity appears to be a conserved feature of activating KIR and may partly explain the slow progress made in identifying their HLA class I ligands. The peptide selectivity of KIR allows NK cells to respond, not only to changes in the surface expression of HLA-C, but also to the more subtle changes in the HLA-C peptidome, such as occur during viral infection and malignant transformation. Here, we review recent advances in understanding of human-specific KIR evolution and how the inhibitory and activating HLA-C receptors allow NK cells to respond to healthy cells, diseased cells, and the semi-allogeneic cells of the fetus.

Indexed as

HaplotypesHLA-C AntigensHumansReceptors, KIRReceptors, KIR2DL1Receptors, Natural Killer CellHLA-C AntigensReceptors, KIRReceptors, KIR2DL1Receptors, Natural Killer CellAntigen presentationGenetic polymorphismHLA class IHost-pathogen interactionsKIRModern human migrationNatural killer cells

Identifiers

PMID28695291
PMCPMC5560170
OpenAlexW2736198333

What OpenQuestion holds

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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.