ReviewBritish journal of clinical pharmacology2011
Delayed drug hypersensitivity: models of T-cell stimulation.
Review in British journal of clinical pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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.
Who cites it
62 citing papers in PubMed, 1 synthesis or guideline pooled it, 160 citations in OpenAlex.
- Clinical pharmacogenetics implementation consortium guidelines for HLA-B genotype and abacavir dosing.Clinical pharmacology and therapeutics · 2012Guideline
- Research progress on potential high-risk drugs for Stevens-Johnson syndrome and toxic epidermal necrolysis with insights from adverse drug reaction database mining.Frontiers in pharmacology · 2026Review
- Article
- Accelerated Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS) Syndrome in Response to TMP-SMX: A Case Report.The American journal of case reports · 2025Article
- Neuromorphic algorithms for brain implants: a review.Frontiers in neuroscience · 2025Review
- COVID-19 and severe cutaneous allergic reactions to sulfonamides.Allergy and asthma proceedings · 2024Article
- Risk factors for drug hypersensitivity reactions in children.Italian journal of pediatrics · 2024Review
- Delayed Type Hypersensitivity Reaction Induced By Liraglutide With Tolerance to Semaglutide.JCEM case reports · 2024Article
- Phenytoin-Induced Toxic Epidermal Necrolysis.Cureus · 2023Article
- Bridging the gap between bench and clinic: the importance of understanding the mechanism of iodinated contrast media hypersensitivity.The British journal of radiology · 2023Review
- Pre-validation study of spectrophotometric direct peptide reactivity assay (Spectro-DPRA) as a modifiedToxicological research · 2022Article
- Whole-Blood 3-Gene Signature as a Decision Aid for Rifapentine-based Tuberculosis Preventive Therapy.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2022Article
- Article
- Unravelling the Proteomics of HLA-B*57:01Journal of personalized medicine · 2022Article
- Bullous pemphigoid: An immune disorder related to aging (Review).Experimental and therapeutic medicine · 2022Review
- A review of hypersensitivity methods to detect immune responses to SARS-CoV-2.Methods in microbiology · 2022Article
- Hypersensitivity reactions to small molecule drugs.Frontiers in immunology · 2022Review
- Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis: A Review of Diagnosis and Management.Medicina (Kaunas, Lithuania) · 2021Review
- Oxidative Stress in Drug-Induced Liver Injury (DILI): From Mechanisms to Biomarkers for Use in Clinical Practice.Antioxidants (Basel, Switzerland) · 2021Review
- CD1a function in human skin disease.Molecular immunology · 2021Review
2 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Drug-induced hypersensitivity reactions can cause a variety of serious diseases by involving drug-specific T-cells. Many of these reactions have been explained by the hapten concept, which postulates that small chemical compounds need to bind covalently to proteins to be recognized by the immune system. Due to their chemical reactivity, haptens stimulate the innate immunity by binding covalently to endogenous proteins and form so called hapten-carrier complexes, which are antigenic and induce T-cell responses. In recent years, a new concept has been developed since drug-induced hypersensitivity reactions were also observed with chemically unreactive drugs. This concept implies direct and reversible interactions of the drug between T-cell receptors (TCR) and major histocompatability complex (MHC) molecules. Therefore it was termed pharmacological interactions with immune receptors (p-i concept). Early observations on drug reacting T-cell clones (TCC) let believe that drugs bind first to the T-cell receptor since HLA molecules could be exchanged without affecting the drug reactivity. However, MHC molecules were always required for full activation of TCC. According to its strong HLA-B*5701 association, recent data on abacavir suggest that a drug could first bind to the peptide binding groove of the MHC molecule. The thereby modified HLA molecule can then be recognized by specific T-cells. Consequently, two types of reactions based on the p-i mechanism may occur: on the one hand, drugs might preferentially bind directly to the TCR, whereas in defined cases with strong HLA association, drugs might bind directly to the MHC molecule.
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Registered trials
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.