Journal
ANNUAL REVIEW OF MEDICINE, VOL 66
Volume 66, Issue -, Pages 439-454Publisher
ANNUAL REVIEWS
DOI: 10.1146/annurev-med-050913-022745
Keywords
altered peptide; human leukocyte antigen; major histocompatibility complex; Stevens-Johnson syndrome; toxic epidermal necrolysis; pharmacogenomics
Categories
Funding
- NHLBI NIH HHS [U19 HL065962] Funding Source: Medline
- NIAID NIH HHS [R01 AI103348] Funding Source: Medline
- NIGMS NIH HHS [P50 GM115305] Funding Source: Medline
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [U19HL065962] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI103348] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [P50GM115305] Funding Source: NIH RePORTER
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The immunological mechanisms driving delayed hypersensitivity reactions (HSRs) to drugs mediated by drug-reactive T lymphocytes are exemplified by several key examples and their human leukocyte antigen (HLA) associations: abacavir and HLA-B*57:01, carbamazepine and HLA-B*15:02, allopurinol and HLA-B*58:01, and both amoxicillin-clavulanate and nevirapine with multiple class I and II alleles. For HLA-restricted drug HSRs, specific class I and/or II HLA alleles are necessary but not sufficient for tissue specificity and the clinical syndrome. Several models have been proposed to explain the immunopathogenesis of severe T cell-mediated drugHSRs, and our increased understanding of the risk factors and mechanisms involved in the development of these reactions will further the development of sensitive and specific strategies for preclinical screening that will lead to safer and more cost-effective drug design.
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