1. Fig. 4. Patho-mechanism of T-cell-mediated reactions and co-stimulators. A shows the Hapten and Pro-hapten hypothesis. In this model, the drug (Piperacillin) is processed intracellularly and presented on the surface of APCs in the complex of MHC class I. Indeed, the drug binds to endogenous peptide or protein by covalent bonds. B shows the P-I model. In this model, the drugs or their metabolites (CBZ or Allopurinol) are able to bind directly to TCR by noncovalent bonds without the intracellular processing of drug. C shows the altered peptide repertoire model. In this model, the drug (abacavir) is able to bind to the MHC (peptide binding groove) and these results in alteration of the peptide repertoire. The costimulators, including viral infections or reactivations, may become involved in the patho-mechanism, accompanied by cross-talk between dendritic cells and natural killer cells [111]. Consequently, different clinical phenotypes of severe cutaneous adverse drug reactions will be formed according to the key cells and cytokines involved. SJS/TEN, Stevens-Johnson syndrome/toxic epidermal necrolysis; HSS/DRESS, hypersensitivity syndrome/drug reaction with eosinophilia and systemic symptoms; AGEP, acute, generalised, exanthematous pustulosis; APC, antigen presenting cell; pDC, plasmacytoid dendritic cell; P-I, pharmacological interaction; KIRs, killer immunoglobulin-like receptors.
Fig. 4. Patho-mechanism of T-cell-mediated reactions and co-stimulators. A shows the Hapten and Pro-hapten hypothesis. In this model, the drug (Piperacillin) is processed intracellularly and presented on the surface of APCs in the complex of MHC class I. Indeed, the drug binds to endogenous peptide…
Asia Pac Allergy. 2019;9:e20.