PD-1 is a protein component (receptor) on the surface of T lymphocytes that, when activated, acts as a suppressor of the immune function of lymphocytes. And PD-L1 on the surface of tumor cells activates PD-1.
Both PD-1 inhibitors and PD-L1 inhibitors block the “close contact” between the two, thus preventing PD-1 from being activated and relieving lymphocytes of their suppression so that they can focus their fire on the tumor. In the process of fighting, if normal cells are mistakenly injured, this can cause adverse effects of the treatment.
Traditional chemotherapy is mostly administered intravenously and works systemically, like a “weapon of mass destruction,” and is less selective, killing tumors while harming normal tissues and cells. Targeted therapy is a treatment targeting specific oncogenic mutations, which is like a “laser-guided artillery shell”, with high hit rate and high power, and very little damage outside the target (less adverse effects). But targeted therapy must have a target – a specific gene mutation – and if there is no mutation, or if the mutation has changed, it won’t work.
A comparison shows that PD-1/PD-L1 inhibitors do not work in the same way as either chemotherapy or targeted therapy, because the latter two are used as weapons to attack the tumor directly, whereas PD-1/PD-L1 inhibitors do not attack the tumor themselves, but work by restoring the body’s immune response to the tumor.
Co-reviewed by: Guangdong Provincial People’s Hospital Guangdong Lung Cancer Institute Dr. Wang Zhen, deputy chief physician Linlin Lai