| Immunotherapy Class |
Example Agents |
Primary Target |
Core Mechanism |
Interaction Considerations |
Net Effect |
| PD-1 inhibitors |
Nivolumab, Pembrolizumab |
PD-1 receptor on T cells |
Blocks inhibitory PD-1 signaling → restores cytotoxic T-cell activity |
High-dose steroids or strong immunosuppressants may blunt effect; autoimmune risk |
↑ Anti-tumor immune activation |
| PD-L1 inhibitors |
Atezolizumab, Durvalumab |
PD-L1 on tumor/immune cells |
Prevents PD-L1 from engaging PD-1 → enhances T-cell response |
Similar immune-related adverse event (irAE) profile as PD-1 inhibitors |
↑ Immune activation |
| CTLA-4 inhibitors |
Ipilimumab |
CTLA-4 checkpoint |
Enhances early T-cell priming in lymph nodes |
Higher autoimmune toxicity risk vs PD-1 class |
↑ T-cell priming |
| CAR-T therapy |
CD19 CAR-T products |
Tumor antigen (e.g., CD19) |
Genetically engineered T cells directly target tumor cells |
Risk of cytokine release syndrome (CRS) and neurotoxicity |
Direct immune-mediated tumor killing |
| Monoclonal antibodies (non-checkpoint) |
Trastuzumab, Rituximab |
Specific tumor antigens |
Antibody-dependent cellular cytotoxicity (ADCC) or receptor blockade |
Combination with chemo common; immune activation depends on Fc engagement |
Targeted immune-mediated killing |
| Cytokine therapy |
IL-2, IFN-α |
Immune activation pathways |
Stimulates T-cell and NK cell proliferation |
High systemic toxicity; rarely used now vs checkpoint inhibitors |
Broad immune stimulation |
| Cancer vaccines |
mRNA or peptide-based |
Tumor antigens |
Induces tumor-specific immune memory |
Often combined with checkpoint blockade |
Adaptive immune priming |
| Bispecific T-cell engagers |
Blinatumomab |
CD3 + tumor antigen |
Bridges T cells directly to tumor cells |
CRS risk; continuous infusion in some protocols |
Direct T-cell redirection |