Evidence map›Paper›PMID 29171940›Full record

ReviewHLA2018

HLAs: Key regulators of T-cell-mediated drug hypersensitivity.

A J Redwood, R K Pavlos, K D White, E J Phillips

Open access · bronzeAbstract readReview
In one paragraph

Review in HLA, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 3 pooled it
7.1field-weighted citation impact, top 2% 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

48 citing papers in PubMed, 3 syntheses or guidelines pooled it, 99 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Drug hypersensitivity reactions: review of the state of the science for prediction and diagnosis.Toxicological sciences : an official journal of the Society of Toxicology · 2024
    Review
  11. Article
  12. Severe cutaneous adverse reactions.Nature reviews. Disease primers · 2024
    Review
  13. Article
  14. Article
  15. Observational
  16. Review
  17. Review
  18. Genetic Susceptibility ofBiomedicines · 2023
    Article
  19. Impact of Pharmacogenomics in Clinical Practice.Pharmaceuticals (Basel, Switzerland) · 2023
    Review
  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

4 authors at 2 institutions in 2 countries.

A J RedwoodInstitute for Immunology & Infectious Diseases, Murdoch University, Murdoch, Australia.
R K PavlosInstitute for Immunology & Infectious Diseases, Murdoch University, Murdoch, Australia.
K D WhiteDivision of Infectious Diseases, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee.
E J PhillipsInstitute for Immunology & Infectious Diseases, Murdoch University, Murdoch, Australia.
Murdoch University · AUVanderbilt University Medical Center · US

Funding

Tennessee CFAR: Implementation of Culturally Responsive Trauma-Informed Care with Youth with HIV in Memphis, TNP30AI110527 · NIAID · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Stephany Norah Duda · 2015 to 2026
$27.5M
Understanding and preventing HLA-associated drug reactionsP50GM115305 · NIGMS · VANDERBILT UNIVERSITY MEDICAL CENTER · PI PHILLIPS, ELIZABETH · 2015 to 2019
$13.0M
Stevens-Johnson Syndrome/Toxic Epidural Necrolysis 2017: Building Multidisciplinary Networks to Drive Science and TranslationR13AR071267 · NIAMS · VANDERBILT UNIVERSITY MEDICAL CENTER · PI PHILLIPS, ELIZABETH · 2017 to 2017
$43k
NIAID NIH HHS P30 AI110527NIAMS NIH HHS R13 AR071267NIGMS NIH HHS P50 GM115305
6 · The paper itself

Abstract

Adverse drug reactions (ADR) can be broadly categorised as either on-target or off-target. On-target ADRs arise as a direct consequence of the pharmacological properties of the drug and are therefore predictable and dose-dependent. On-target ADRs comprise the majority (>80%) of ADRs, relate to the drug's interaction with its known pharmacological target and are a result of a complex interplay of genetic and ecologic factors. In contrast, off-target ADRs, including immune-mediated ADRs (IM-ADRs), are due to unintended pharmacological interactions such as inadvertent ligation of host cell receptors or non-pharmacological interactions mediated through an adaptive immune response. IM-ADRs can be classified according to the primary immune cell involved and include B-cell-mediated (Gell-Coombs type I-III reactions) and T-cell-mediated (Gell-Coombs type IV or delayed hypersensitivity) reactions. IM-ADRs mediated by T cells are associated with phenotypically distinct clinical diagnoses and can vary from a mild delayed rash to a life-threatening cutaneous, systemic or organ disease, such as Stephen Johnson syndrome/toxic epidermal necrolysis, drug reaction with eosinophilia and systemic symptoms and drug-induced liver disease. T-cell-mediated ADRs are strongly linked to the carriage of particular HLA risk alleles which are in the case of abacavir hypersensitivity and HLA-B*57:01 has led to translation into the clinic as a routine screening test. In this review, we will discuss the immunogenetics and pathogenesis of IM-ADRs and how HLA associations inform both pre-drug screening strategies and mechanistic understanding.

Indexed as

Immunity, CellularAbacavirB-LymphocytesDideoxynucleosidesDrug HypersensitivityHLA-B AntigensHumansRisk FactorsT-LymphocytesAbacavirDideoxynucleosidesHLA-B*57:01 antigenHLA-B Antigensabacaviradverse drug reactionallopurinolangioedemaaspirin exacerbated respiratory diseasecarbamazepineHLAimmunological memorypharmacogenomics

Identifiers

PMID29171940
PMCPMC5743596
OpenAlexW2769962798

What OpenQuestion holds

Textmetadata
LicenceTDM
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.