Letter to the editor
Immunologic 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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    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].

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  • Allotype specific interactions of drugs and HLA molecules in hypersensitivity reactions

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    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•].

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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.

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