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Annu Rev Med. 2015;66:439-54. doi: 10.1146/annurev-med-050913-022745. Epub 2014 Oct 27.

T cell-mediated hypersensitivity reactions to drugs.

Author information

1
Institute for Immunology and Infectious Diseases, Murdoch University, Murdoch, Western Australia, 6150; email: e.phillips@iiid.com.au.

Abstract

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, allo-purinol 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 drug HSRs, 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.

KEYWORDS:

Stevens-Johnson syndrome; altered peptide; human leukocyte antigen; major histocompatibility complex; pharmacogenomics; toxic epidermal necrolysis

PMID:
25386935
PMCID:
PMC4295772
DOI:
10.1146/annurev-med-050913-022745
[Indexed for MEDLINE]
Free PMC Article

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