Final answer:
Removing the blockage between PD-1 and PD-L1 unleashes T-cells to attack cancer cells by preventing PD-1 from inhibiting T-cell activation. However, there's a risk that T-cells may also destroy healthy cells expressing PD-L1. Dosage and frequency of PD-L1 inhibitors must be carefully managed to maximize cancer cell targeting while minimizing harm to healthy cells.
Step-by-step explanation:
Why does removing the blockage between PD-1 and PD-L1 result in T-cell activation against cancer cells? The removal results in T-cell activation because PD-1 is a protein that naturally inhibits T-cell action when it binds to PD-L1, a process that cancer cells exploit to protect themselves. By disrupting this interaction, checkpoint inhibitors allow T-cells to recognize and destroy cancer cells.
If healthy cells express PD-L1, what happens when PD-1/PD-L1 blockage occurs with immunotherapy? T-cells may destroy healthy cells which present PD-L1 as well, leading to potential side effects known as 'immune-related adverse events'.
How does the dosage and frequency of PD-L1 inhibitors like Atezolizumab impact T-cell activity against cancer cells and healthy cells? Dosage and frequency can influence T-cell specificity and reactivity; too much can lead to an overactive immune response affecting both cancerous and healthy cells, while controlled dosing attempts to minimize such effects and target only cancer cells.