Description: <pre>
Immunotherapy is not one drug class. It includes:
-Immune checkpoint inhibitors (PD-1, PD-L1, CTLA-4)
-CAR-T therapies
-Monoclonal antibodies
-Cytokine therapies (IL-2, IFN-α)
-Cancer vaccines
-Bispecific T-cell engagers
</pre>
<b>PD-1 blockade antibody therapy</b> is one of the cornerstone approaches in modern cancer immunotherapy.<br>
Under normal physiological conditions, when PD-1 binds to its ligands (PD-L1 or PD-L2) on other cells, it functions as a "checkpoint" to reduce overly active T cell responses and prevent autoimmunity.<br>
PD-1 blockade therapies involve monoclonal antibodies that target either PD-1 or its ligand PD-L1.<br>
• By blocking the interaction between PD-1 and its ligands, these antibodies effectively release the "brakes" on T cells.<br>
• The re-activated T cells can then recognize and destroy cancer cells more efficiently.<br>
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<!-- Immunotherapy — Mechanism & Interaction Mini-Table -->
<table border="1" cellpadding="4" cellspacing="0">
<tr>
<th>Immunotherapy Class</th>
<th>Example Agents</th>
<th>Primary Target</th>
<th>Core Mechanism</th>
<th>Interaction Considerations</th>
<th>Net Effect</th>
</tr>
<tr>
<td><b>PD-1 inhibitors</b></td>
<td>Nivolumab, Pembrolizumab</td>
<td>PD-1 receptor on T cells</td>
<td>Blocks inhibitory PD-1 signaling → restores cytotoxic T-cell activity</td>
<td>High-dose steroids or strong immunosuppressants may blunt effect; autoimmune risk</td>
<td><b>↑ Anti-tumor immune activation</b></td>
</tr>
<tr>
<td><b>PD-L1 inhibitors</b></td>
<td>Atezolizumab, Durvalumab</td>
<td>PD-L1 on tumor/immune cells</td>
<td>Prevents PD-L1 from engaging PD-1 → enhances T-cell response</td>
<td>Similar immune-related adverse event (irAE) profile as PD-1 inhibitors</td>
<td><b>↑ Immune activation</b></td>
</tr>
<tr>
<td><b>CTLA-4 inhibitors</b></td>
<td>Ipilimumab</td>
<td>CTLA-4 checkpoint</td>
<td>Enhances early T-cell priming in lymph nodes</td>
<td>Higher autoimmune toxicity risk vs PD-1 class</td>
<td><b>↑ T-cell priming</b></td>
</tr>
<tr>
<td><b>CAR-T therapy</b></td>
<td>CD19 CAR-T products</td>
<td>Tumor antigen (e.g., CD19)</td>
<td>Genetically engineered T cells directly target tumor cells</td>
<td>Risk of cytokine release syndrome (CRS) and neurotoxicity</td>
<td><b>Direct immune-mediated tumor killing</b></td>
</tr>
<tr>
<td><b>Monoclonal antibodies (non-checkpoint)</b></td>
<td>Trastuzumab, Rituximab</td>
<td>Specific tumor antigens</td>
<td>Antibody-dependent cellular cytotoxicity (ADCC) or receptor blockade</td>
<td>Combination with chemo common; immune activation depends on Fc engagement</td>
<td><b>Targeted immune-mediated killing</b></td>
</tr>
<tr>
<td><b>Cytokine therapy</b></td>
<td>IL-2, IFN-α</td>
<td>Immune activation pathways</td>
<td>Stimulates T-cell and NK cell proliferation</td>
<td>High systemic toxicity; rarely used now vs checkpoint inhibitors</td>
<td><b>Broad immune stimulation</b></td>
</tr>
<tr>
<td><b>Cancer vaccines</b></td>
<td>mRNA or peptide-based</td>
<td>Tumor antigens</td>
<td>Induces tumor-specific immune memory</td>
<td>Often combined with checkpoint blockade</td>
<td><b>Adaptive immune priming</b></td>
</tr>
<tr>
<td><b>Bispecific T-cell engagers</b></td>
<td>Blinatumomab</td>
<td>CD3 + tumor antigen</td>
<td>Bridges T cells directly to tumor cells</td>
<td>CRS risk; continuous infusion in some protocols</td>
<td><b>Direct T-cell redirection</b></td>
</tr>
</table>