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. Author manuscript; available in PMC: 2016 Dec 1.
Published in final edited form as: Curr Opin Infect Dis. 2016 Dec;29(6):561–576. doi: 10.1097/QCO.0000000000000323

Figure 1. Heading: Schematic of proposed T-cell-mediated ADR pathogenesis theories.

Figure 1

(i) The hapten/prohapten model is where an antigen (e.g. antibiotic) covalently binds to a self-peptide, is intracellularly processed and then presented with MHC to T cells as a ‘foreign antigen’ [51,52]. An example of the hapten/prohapten model is when penicillin G derivatives bind lysine residues on serum albumin [53–55].

(ii) The p-i concept (the pharmacological interaction with immune receptor) is based upon non-covalent binding of antigens to HLA or TCR without immune processing, explaining how reactions can occur upon first presentation [51,56].

(iii) The ‘altered self-repertoire model’ is based upon drug models (e.g. abacavir) that demonstrated that drugs can occupy positions in the peptide binding groove of the MHC, altering the binding cleft and subsequently the specificity of MHC binding [57–59]. Source: [51,52], [53–55], [51,56], [57–59].