Active suppression rather than ignorance: tolerance to abacavir-induced HLA-B*57:01 peptide repertoire alteration
Elizabeth J. Phillips and Simon A. Mallal
Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA. Institute for Immunology and Infectious Diseases, Murdoch University, Murdoch, Western Australia.
Address correspondence to: Elizabeth J. Phillips, 1161 – 21 St. Avenue South, A-2200 Medical Center North, Nashville, Tennessee 37232-2582, USA. Phone: 615.322.9174; Email: elizabeth.j.phillips@vanderbilt.edu.
Find articles by Phillips, E. in: JCI | PubMed | Google Scholar
Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA. Institute for Immunology and Infectious Diseases, Murdoch University, Murdoch, Western Australia.
Address correspondence to: Elizabeth J. Phillips, 1161 – 21 St. Avenue South, A-2200 Medical Center North, Nashville, Tennessee 37232-2582, USA. Phone: 615.322.9174; Email: elizabeth.j.phillips@vanderbilt.edu.
Find articles by Mallal, S. in: JCI | PubMed | Google Scholar
First published May 21, 2018 - More info
J Clin Invest. 2018;128(7):2746–2749. https://doi.org/10.1172/JCI121525.
Copyright © 2018, American Society for Clinical Investigation
The discovery of HLA-B*57:01–associated abacavir hypersensitivity is a translational success story that eliminated adverse reactions to abacavir through pretreatment screening and defined a mechanistic model of an altered peptide repertoire. In this issue of the JCI, Cardone et al. have developed an HLA-B*57:01–transgenic mouse model and demonstrated that CD4+ T cells play a key role in mediating tolerance to the dramatically altered endogenous peptide repertoire induced by abacavir and postulate a known mechanism by which CD4+ T cells suppress DC maturation. This report potentially explains why 45% of HLA-B*57:01 carriers tolerate abacavir and provides a framework for future studies of HLA-restricted, T cell–mediated drug tolerance and hypersensitivity.
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