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Structural Elements Recognized by Abacavir-Induced T Cells.

Daniel Yerly1, Yuri Andreiw Pompeu2, Ryan J Schutte3

  • 1Department of Rheumatology, Immunology and Allergology, University Hospital of Bern, 3010 Bern, Switzerland. daniel.yerly@allergy.unibe.ch.

International Journal of Molecular Sciences
|July 8, 2017
PubMed
Summary
This summary is machine-generated.

Adverse drug reactions are linked to human leukocyte antigen (HLA) alleles. This study found that T cells recognizing abacavir hypersensitivity can cross-react with viral peptides due to structural similarities in HLA-presented complexes.

Keywords:
Human Leukocyte Antigencrystallographydrug hypersensitivity

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Area of Science:

  • Immunology
  • Pharmacogenomics
  • Structural Biology

Background:

  • Adverse drug reactions (ADRs) are a major global health concern, with human leukocyte antigen (HLA) alleles strongly implicated in drug hypersensitivities.
  • Drug-specific T cell receptors (TCRs) recognize peptide/HLA complexes, but the structural features of these peptides, especially in relation to small molecule drugs, remain poorly understood.

Purpose of the Study:

  • To investigate the structural similarities of HLA-presented peptides recognized by drug-specific TCRs using abacavir hypersensitivity as a model.
  • To determine if viral peptides with similar structural motifs can stimulate T cell responses in the context of HLA-B*57:01 and abacavir.

Main Methods:

  • Utilized the crystal structure of HLA-B*57:01 complexed with abacavir and a self-peptide to identify potential drug-specific TCR recognition motifs.
  • Analyzed viral sequences for structural similarities to the immunogenic self-peptide.
  • Employed abacavir-specific T cell clones to assess responsiveness to virus-derived peptides presented by HLA-B*57:01.

Main Results:

  • Identified flexible and solvent-exposed peptide side chains as potential recognition motifs for drug-specific TCRs.
  • Found a viral peptide (VTQQAQVRL, HSV1/2 230-238) that stimulated an abacavir-specific T cell clone in the context of HLA-B*57:01.
  • Demonstrated that T cell responses to abacavir involve subsets recognizing both self and cross-reactive viral peptides.

Conclusions:

  • The polyclonal T cell response to abacavir includes T cells that recognize self-peptide/HLA-B*57:01 complexes.
  • These T cells can cross-react with viral peptide/HLA-B*57:01 complexes due to conserved TCR contact residues.
  • This cross-reactivity mechanism offers insights into the pathogenesis of drug hypersensitivity and potential autoimmune responses.