Evidence map›Paper›PMID 26307125›Full record

Trial reportClinical and experimental immunology2015

Polymorphisms within the human leucocyte antigen-E gene and their associations with susceptibility to rheumatoid arthritis as well as clinical outcome of anti-tumour necrosis factor therapy.

M Iwaszko, J Świerkot, K Kolossa, S Jeka, P Wiland, K Bogunia-Kubik

Abstract readClinical TrialComparative Study
In one paragraph

Trial report in Clinical and experimental immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

24 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
  3. Article
  4. Review
  5. Review
  6. Pharmacogenomics of TNF inhibitors.Frontiers in immunology · 2025
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Shared epitope and polymorphism ofCentral-European journal of immunology · 2021
    Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. The genetic contribution ofAnnals of translational medicine · 2019
    Article
  19. Dimorphism of HLA-E and its Disease Association.International journal of molecular sciences · 2019
    Review
  20. Towards Clinical Translation of CD8International journal of molecular sciences · 2019
    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

6 authors.

M IwaszkoLaboratory of Clinical Immunogenetics and Pharmacogenetics, L. Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Wroclaw, Poland.
J ŚwierkotDepartment of Rheumatology and Internal Medicine, Wroclaw Medical University, Wroclaw.
K KolossaClinical Department of Rheumatology and Connective Tissue Diseases, Hospital University Number 2 Jana Biziela, Bydgoszcz, Poland.
S JekaClinical Department of Rheumatology and Connective Tissue Diseases, Hospital University Number 2 Jana Biziela, Bydgoszcz, Poland.
P WilandDepartment of Rheumatology and Internal Medicine, Wroclaw Medical University, Wroclaw.
K Bogunia-KubikLaboratory of Clinical Immunogenetics and Pharmacogenetics, L. Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Wroclaw, Poland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Involvement of the non-classical human leucocyte antigen-E (HLA-E) in both innate and acquired immune response suggests its possible role in development of autoimmune pathologies. This study was undertaken to investigate relationships between the HLA-E gene single nucleotide polymorphisms (SNPs) and a risk of rheumatoid arthritis (RA), as well as to evaluate a potential of these polymorphisms to modulate clinical outcome of anti-tumour necrosis factor (TNF) treatment in female patients. A total of 223 female patients with RA receiving anti-TNF biological therapy and 134 female healthy subjects were enrolled into the study. Genotypings for two SNPs within the HLA-E gene (rs1264457 HLA-E*01:01/01:03; rs1059510 HLA-E*01:03:01/01:03:02) were performed using a polymerase chain reaction (PCR) amplification employing LightSNiP assays. Clinical response was evaluated according to the European League Against Rheumatism (EULAR) criteria at 12 and 24 weeks after initiation of the therapy. The frequency of the HLA-E*01:01/01:01 genotype was decreased significantly in RA patients in comparison to controls (P = 0.031). The presence of the HLA-E*01:01/01:01 genotype in patients correlated with better EULAR response after 12 weeks of anti-TNF treatment, while 01:03 allele carriers were generally unresponsive to the treatment (P = 0.014). The HLA-E*01:03/01:03 genotype was also over-represented among non-responding patients in comparison to HLA-E*01:01/01:01 homozygotes (P = 0.021). With respect to the HLA-E rs1059510 variation, a better response after 12 weeks was observed more frequently in patients carrying the HLA-E*01:03:01/01:03:01 genotype than other genotypes (P = 0.009). The results derived from this study imply that HLA-E polymorphisms may influence RA susceptibility and affect clinical outcome of anti-TNF therapy in female RA patients.

Indexed as

Arthritis, RheumatoidGenetic Predisposition to DiseaseGenotypeHistocompatibility Antigens Class IPolymorphism, Single NucleotideAdultFemaleHLA-E AntigensHumansMiddle AgedTime FactorsTumor Necrosis Factor-alphaHistocompatibility Antigens Class IHLA-E AntigensTumor Necrosis Factor-alphaanti-TNF therapyHLA-E polymorphismrheumatoid arthritisTNF inhibitors

Identifiers

PMID26307125
PMCPMC4636889

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Registered trials

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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.