Immunology · Immunosuppressants, biologics, checkpoint inhibitors, and antiretroviral drugs
By completing this question set, you will be able to trace the corticosteroid mechanism from receptor binding through gene transcription modulation to its anti-inflammatory and immunosuppressive effects, and predict the complications of chronic use. You will map the calcineurin inhibitor pathway (binding protein → calcineurin → NFAT → IL-2) for both cyclosporine and tacrolimus, distinguish their toxicity profiles, and explain why sirolimus targets mTOR instead of calcineurin despite binding the same protein (FKBP-12). You will describe the antimetabolites (azathioprine, mycophenolate, methotrexate) by mechanism, predict drug interactions (allopurinol-azathioprine), and explain lymphocyte selectivity. You will classify biologic agents by their target (anti-cytokine vs cell-targeted vs co-stimulation blocker vs checkpoint inhibitor), explain why anti-TNF-α agents require TB screening, and predict immune-related adverse events from checkpoint inhibitor mechanism. You will distinguish co-stimulation blockade (abatacept — promotes tolerance) from checkpoint inhibition (ipilimumab — disrupts tolerance) as opposite applications of the same co-stimulatory biology. Finally, you will describe ART drug class mechanisms in pharmacologic detail, identify drug-specific toxicities, and explain pharmacogenomic testing requirements.