Evidence map›Paper›PMID 29614084›Full record

Trial reportPloS one2018

Identification of HLA-DRB1 association to adalimumab immunogenicity.

Mohan Liu, Jacob Degner, Justin Wade Davis, Kenneth B Idler, Ahmed Nader, Nael M Mostafa, Jeffrey F Waring

Open access · goldAbstract readClinical Trial, Phase III
In one paragraph

Trial report in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
10.1field-weighted citation impact, top 1% 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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 80 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Review
  5. Classical HLA Allele and Haplotype Frequency Estimates in US Populations.bioRxiv : the preprint server for biology · 2026
    Article
  6. Genomic Impacts of Biological Exposures.Journal of developmental biology · 2026
    Review
  7. Observational
  8. Review
  9. Review
  10. Article
  11. Article
  12. Pharmacogenomics of TNF inhibitors.Frontiers in immunology · 2025
    Review
  13. Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. 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

7 authors at 1 institution in 1 country.

Mohan LiuPharmacogenetics and Human Genetics, Genomics Research Center, AbbVie Inc., North Chicago, IL, United States of America.ORCID 0000-0003-0653-7397
Jacob DegnerPharmacogenetics and Human Genetics, Genomics Research Center, AbbVie Inc., North Chicago, IL, United States of America.
Justin Wade DavisPharmacogenetics and Human Genetics, Genomics Research Center, AbbVie Inc., North Chicago, IL, United States of America.
Kenneth B IdlerPharmacogenetics and Human Genetics, Genomics Research Center, AbbVie Inc., North Chicago, IL, United States of America.
Ahmed NaderClinical Pharmacology and Pharmacometrics, AbbVie Inc., North Chicago, IL, United States of America.
Nael M MostafaClinical Pharmacology and Pharmacometrics, AbbVie Inc., North Chicago, IL, United States of America.
Jeffrey F WaringPharmacogenetics and Human Genetics, Genomics Research Center, AbbVie Inc., North Chicago, IL, United States of America.
AbbVie (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Anti-drug antibody formation occurs with most biological agents across disease states, but the mechanism by which they are formed is unknown. The formation of anti-drug antibodies to adalimumab (AAA) may decrease its therapeutic effects in some patients. HLA alleles have been reported to be associated with autoantibody formation against interferons and other TNF inhibitors, but not adalimumab. We analyzed samples from 634 subjects with either rheumatoid arthritis (RA) or hidradenitis suppurativa (HS): 37 subjects (17 RA and 20 HS) developed AAA (AAA+) during adalimumab treatment and 597 subjects (348 RA, 249 HS) did not develop AAA (AAA-) during the clinical trials. Using next-generation sequencing-based HLA typing, we identified three protective HLA alleles (HLA-DQB1*05, HLA-DRB1*01,and HLA-DRB1*07) that were less prevalent in AAA+ than AAA-subjects (ORs: 0.4, 0.25 and 0.28, respectively; and P values: 0.012, 0.012 and 0.018, respectively) and two risk HLA alleles (HLA-DRB1*03 and HLA-DRB1*011) that were more abundant in AAA+ than AAA-subjects (ORs: 2.52, and 2.64, respectively; and P values: 0.006 and 0.019). Similar to the finding of Billiet et al. who found that carriage of the HLA-DRB1*03 allele was more prevalent in those with anti-infliximab antibodies (OR = 3.6, p = 0.002, 95% CI: [1.5,8.6]).), we found HLA-DRB1*03 allele was also more prevalent in anti-adalimumab positive (OR = 2.52, p = 0.006, 95% CI: [1.37,4.63]). The results suggest that specific HLA alleles may play a key role in developing AAAs in RA and HS patients treated with adalimumab.

Indexed as

AdalimumabAllelesAnti-Inflammatory AgentsAntirheumatic AgentsArthritis, RheumatoidHidradenitis SuppurativaHistocompatibility TestingHLA-DQ beta-ChainsHLA-DRB1 ChainsHumansPharmacogenomic VariantsSequence AnalysisAdalimumabAnti-Inflammatory AgentsAntirheumatic AgentsHLA-DQB1 antigenHLA-DQ beta-ChainsHLA-DRB1 Chains

Identifiers

PMID29614084
PMCPMC5882140
OpenAlexW2795694659

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.