Evidence map›Paper›PMID 31820163›Full record

ReviewCurrent diabetes reports2019

What the HLA-I!-Classical and Non-classical HLA Class I and Their Potential Roles in Type 1 Diabetes.

Rebecca C Wyatt, Giacomo Lanzoni, Mark A Russell, Ivan Gerling, Sarah J Richardson

Open access · hybridAbstract readReview
In one paragraph

Review in Current diabetes reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 9% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. From bats to humans: uncoveringbioRxiv : the preprint server for biology · 2026
    Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. Multiple Sclerosis: Inflammatory and Neuroglial Aspects.Current issues in molecular biology · 2023
    Review
  20. Review
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

5 authors at 3 institutions in 2 countries.

Rebecca C WyattInstitute of Biomedical and Clinical Science, University of Exeter Medical School, RILD Building, Barrack Road, Exeter, EX2 5DW, UK.
Giacomo LanzoniDiabetes Research Institute, University of Miami - Miller School of Medicine, 1450 NW 10th Avenue, Miami, FL, 33136, USA.
Mark A RussellInstitute of Biomedical and Clinical Science, University of Exeter Medical School, RILD Building, Barrack Road, Exeter, EX2 5DW, UK.
Ivan GerlingDepartment of Medicine University of Tennessee Health Science Center and VA Medical Center Research Service, 1030 Jefferson Avenue, Memphis, TN, 38128, USA.
Sarah J RichardsonInstitute of Biomedical and Clinical Science, University of Exeter Medical School, RILD Building, Barrack Road, Exeter, EX2 5DW, UK. s.richardson@exeter.ac.uk.
University of Exeter · GBUniversity of Miami · USUniversity of Tennessee Health Science Center · US

Funding

Defining Islet Heterogeneity Using Single Islet TranscriptomicsUC4DK104155 · NIDDK · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI CAMPBELL-THOMPSON, MARTHA, GERLING, IVAN C · 2014 to 2014
$1.6M
Medical Research Council MR/P010695/1NIDDK NIH HHS UC4 DK104155
6 · The paper itself

Abstract

purpose of reviewHyperexpression of classical HLA class I (HLA-I) molecules in insulin-containing islets has become a widely accepted hallmark of type 1 diabetes pathology. In comparison, relatively little is known about the expression, function and role of non-classical subtypes of HLA-I. This review focuses on the current understanding of the non-classical HLA-I subtypes: HLA-E, HLA-F and HLA-G, within and outside the field of type 1 diabetes, and considers the possible impacts of these molecules on disease etiology. RECENT

findingsEvidence is growing to suggest that non-classical HLA-I proteins are upregulated, both at the RNA and protein levels in the pancreas of individuals with recent-onset type 1 diabetes. Moreover, associations between non-classical HLA-I genotypes and age at onset of type 1 diabetes have been reported in some studies. As with classical HLA-I, it is likely that hyperexpression of non-classical HLA-I is driven by the release of diffusible interferons by stressed β cells (potentially driven by viral infection) and exacerbated by release of cytokines from infiltrating immune cells. Non-classical HLA-I proteins predominantly (but not exclusively) transduce negative signals to immune cells infiltrating at the site of injury/inflammation. We propose a model in which the islet endocrine cells, through expression of non-classical HLA-I are fighting back against the infiltrating immune cells. By inhibiting the activity and function on NK, B and select T cells, the non-classical HLA-I, proteins will reduce the non-specific bystander effects of inflammation, while at the same time still allowing the targeted destruction of β cells by specific islet-reactive CD8+ T cells.

Indexed as

B-LymphocytesCD8 AntigensDiabetes Mellitus, Type 1Histocompatibility Antigens Class IHLA-E AntigensHLA-G AntigensHumansInflammationInsulin-Secreting CellsIslets of LangerhansKiller Cells, NaturalT-LymphocytesUp-RegulationCD8 AntigensHistocompatibility Antigens Class IHLA-E AntigensHLA-F antigensHLA-G AntigensHLA-EHLA-FHLA-GHLA-IImmune systemNon-classical HLA-IType 1 diabetes

Identifiers

PMID31820163
PMCPMC6901423
OpenAlexW2974333724

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.