Letter to the editorImmunologic basis for allopurinol-induced severe cutaneous adverse reactions: HLA-B*58:01-restricted activation of drug-specific T cells and molecular interaction
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Cited by (42)
HLA-B58.01 and allopurinol hypersensitivity renal vasculitis in a Chinese patient
2022, Revue de Medecine InterneThe Function of HLA-B*13:01 Involved in the Pathomechanism of Dapsone-Induced Severe Cutaneous Adverse Reactions
2018, Journal of Investigative DermatologyImmune Mechanisms of Drug Allergy
2018, Drug Allergy TestingHuman leukocyte antigen and idiosyncratic adverse drug reactions
2017, Drug Metabolism and PharmacokineticsCitation Excerpt :However, the inhibitory effect seen with ximelagatran [52] and enhanced effect by lapatinib [103] confuse the situation and provide little information on the underlying mechanism of hypersensitivity. Surface plasmon resonance (SPR) can measure the small molecule binding response to protein as Resonance Units [9,91]. Wei et al. purified HLAs, β-microglobulin, and endogenous peptide from the culture medium of APCs expressing the risk allele and elegantly showed carbamazepine binds directly to HLA-B*15:02; however, the same was not seen with other HLA-B recombinant proteins [9].
Immune Mechanisms of Drug Allergy
2017, Drug Allergy TestingAllotype specific interactions of drugs and HLA molecules in hypersensitivity reactions
2016, Current Opinion in ImmunologyCitation Excerpt :The observed concentration dependence of OXP responses [15,16] correlates with the increased risk and poor prognosis of ALP hypersensitivity in HLA-B*58:01+ patients experiencing renal impairment, where reduced OXP clearance results in higher serum levels and prolonged retention [14•,19••]. Current evidence suggests that ALP/OXP T cells recognise drug presented by a p.i. mechanism, with reports supporting the key characteristics of labile interaction with HLA and absence of intracellular metabolism or antigen processing [17,18•]. However site directed mutagenesis of HLA-B*58:01 indicated that an Arg97Val substitution (one of four differences that distinguishes the antigen-binding cleft of HLA-B*58:01 from HLA-B*57:01), reduces T cell activation suggesting that the binding site for OXP is influenced by or within the antigen-binding cleft [18•].
Supported by grants from the Academia Sinica (40-05-GMMAS-99-TP-B12), the National Science Council (NSC100-2319-B-001-001), and the NRPB project (NSC-101-2325-B001-006 and NSC-102-2325-B001-006).
Disclosure of potential conflict of interest: Y.-T. Chen is a member of a scientific advisory board and has a patent and has received royalties relating to risk assessment for adverse drug reactions. The rest of the authors declare that they have no relevant conflicts of interest.