Drug‐specific CD4<sup>+</sup>T‐cell immune responses are responsible for antituberculosis drug‐induced maculopapular exanthema and drug reaction with eosinophilia and systemic symptoms syndrome

Ye, Y.‐M.; Hur, Gyu Young; Kim, Seung Hyun; Ban, Ga‐Young; Jee, Young Koo; Naisbitt, Dean J.; Park, Hae‐Sim

doi:10.1111/bjd.14839

Cited by 45 publications

(29 citation statements)

References 28 publications

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“…However, in the context of certain mutations in HLA genes, drug–protein conjugation occurs and the conjugates are presented on the surface of antigen-presenting cells, which may activate T cell responses leading to hepatocyte damage of immune origin. Treatment of drug-specific T cells isolated from patients suffering from adverse effects brought on by co-treatment with rifampicin and isoniazid with MHC I and II neutralizing antibodies block the activation of Tcells, suggesting an influential role of HLA patient-specific genotypes in AT-DILI [86]. …”

Section: Specific Molecular Mechanisms Of Isoniazid/rifampicin-inducementioning

confidence: 99%

Genetic Variations Associated with Anti-Tuberculosis Drug-Induced Liver Injury

Bao

Rasmussen

et al. 2018

Curr Pharmacol Rep

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Purpose of this Review In order to combat the development of drug resistance, the clinical treatment of tuberculosis requires the combined use of several anti-tuberculosis (anti-TB) drugs, including isoniazid and rifampicin. Combinational treatment approaches are suggested by the World Health Organization (WHO) and are widely accepted throughout the world. Unfortunately, a major side effect of the treatment is the development of anti-tuberculosis drug-induced liver injury (AT-DILI). Many factors contribute to isoniazid- and rifampicin-mediated AT-DILI and genetic variations are among the most common factors. The purpose of this review is to provide information on genetic variations associated with isoniazid- and rifampicin-mediated AT-DILI. Recent Findings The genetic variations associated with AT-DILI have been identified in the genomic regions within or near genes encoding proteins in the following pathways: drug metabolizing enzymes (NAT2, CYP2E1, and GSTs), accumulation of bile acids, lipids, and heme metabolites (CYP7A1, BSEP, UGTs, and PXR), immune adaptation (HLAs and TNF-α), and oxidant challenge (TXNRD1, SOD1, BACH1, and MAFK). Summary The information summarized in this review considers the genetic bases of risk factors contributing to AT-DILI and provides information that may help for future studies. Some of the implicated genetic variations can be used in the design of genetic tests and serve as biomarkers for the prediction of isoniazid- and rifampicin-mediated AT-DILI risk in personalized medicine.

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Section: Specific Molecular Mechanisms Of Isoniazid/rifampicin-inducementioning

confidence: 99%

Genetic Variations Associated with Anti-Tuberculosis Drug-Induced Liver Injury

Bao

Rasmussen

et al. 2018

Curr Pharmacol Rep

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“…There has been an association reported in Korean patients with DRESS for the class I allele HLA‐C*04:01, which extends to the haplotype HLA‐A*11:01‐B*15:01‐C*04:01. However, these alleles are not reported in the cases presented by Ye et al ., providing evidence that other class II HLA alleles may be important.…”

mentioning

confidence: 60%

“…The study by Ye et al . provides insight into the mechanism of ATD‐associated adverse reactions supporting a role of drug‐specific CD4 + T cells in the pathogenesis.…”

mentioning

confidence: 92%

“…However, the specificity and sensitivity of patch testing is dependent on both the host and the offending drug and few validation studies exist. In the cases presented by Ye et al . patch testing is shown to be of little utility in DRESS and is unsuitable for cases of MPE; however, the oral provocation test and lymphocyte transformation test show a stronger correlation and support multiple drug reactivity.…”

mentioning

confidence: 97%

“…In this issue of the BJD , Ye et al . present data on T‐cell‐specific responses in patients with antituberculosis drug (ATD)‐induced maculopapular exanthema (MPE) and drug reaction with eosinophilia and systemic symptoms (DRESS).…”

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confidence: 99%

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AdDRESSing T‐cell responses to antituberculous drugs

2017

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Variation of clinical manifestations according to culprit drugs in DRESS syndrome

Sim

Jeong

et al. 2019

Pharmacoepidemiology and Drug

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Purpose Drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome is a rare but serious condition that systematically damages various internal organs through T‐cell–mediated immunological drug reactions. We aimed to investigate whether clinical manifestations of DRESS syndrome differ according to culprit drugs. Methods We retrospectively analyzed data from 123 patients with probable/definite DRESS syndrome based on the RegiSCAR criteria (January 2011 to July 2016). The data were obtained from the Korean Severe Cutaneous Adverse Reaction Registry. Causality was assessed using the World Health Organization‐Uppsala Monitoring Centre criteria. The culprit drugs were categorized as allopurinol, carbamazepine, anti‐tuberculosis drug, vancomycin, cephalosporins, dapsone, and nonsteroidal anti‐inflammatory drugs. Results Differences were observed among culprit drugs regarding the frequencies of hepatitis (P < 0.01), renal dysfunction (P < 0.0001), lymphadenopathy (P < 0.01), and atypical lymphocyte (P < 0.01). Latency period differed among culprit drugs (P < 0.0001), being shorter in vancomycin and cephalosporin. In terms of clinical severity, admission duration (P < 0.01) and treatment duration (P < 0.05) differed among culprit drugs, being longer in vancomycin and anti‐tuberculosis drugs, respectively. Conclusions Based on the findings, clinical manifestations, including latency period and clinical severity, may differ according to culprit drugs in DRESS syndrome.

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Drug‐specific CD4⁺T‐cell immune responses are responsible for antituberculosis drug‐induced maculopapular exanthema and drug reaction with eosinophilia and systemic symptoms syndrome

Abstract: This study identifies the presence of isoniazid/rifampicin-specific T cells in patients with ATD-induced maculopapular exanthema and DRESS. Furthermore, it highlights the important role of drug-specific T-cell immune responses in the pathogenesis of these reactions.

Cited by 45 publications

References 28 publications

Genetic Variations Associated with Anti-Tuberculosis Drug-Induced Liver Injury

Genetic Variations Associated with Anti-Tuberculosis Drug-Induced Liver Injury

AdDRESSing T‐cell responses to antituberculous drugs

Variation of clinical manifestations according to culprit drugs in DRESS syndrome

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Drug‐specific CD4+T‐cell immune responses are responsible for antituberculosis drug‐induced maculopapular exanthema and drug reaction with eosinophilia and systemic symptoms syndrome

Abstract: This study identifies the presence of isoniazid/rifampicin-specific T cells in patients with ATD-induced maculopapular exanthema and DRESS. Furthermore, it highlights the important role of drug-specific T-cell immune responses in the pathogenesis of these reactions.

Cited by 45 publications

References 28 publications

Genetic Variations Associated with Anti-Tuberculosis Drug-Induced Liver Injury

Genetic Variations Associated with Anti-Tuberculosis Drug-Induced Liver Injury

AdDRESSing T‐cell responses to antituberculous drugs

Variation of clinical manifestations according to culprit drugs in DRESS syndrome

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Product

Resources

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Drug‐specific CD4⁺T‐cell immune responses are responsible for antituberculosis drug‐induced maculopapular exanthema and drug reaction with eosinophilia and systemic symptoms syndrome