**4. Possible mechanism of action of anti-programme death receptor-1/ Ligand-1 (PD-1/PD-L1) in cancer**

PD-1/PD-L1 is known to control the induction and maintenance of immune tolerance within the tumor microenvironment. It performs a significant role in cytotoxic secretion and T cell activation and proliferation in cancer to inhibit antitumor immune responses in host [41]. During tumor proliferation, the PD-L1 is highly expressed on tumor cells that bind to the PD-1 receptor on T cells that receive an inhibitory signal from the PD-L1 binding i.e. to inhibit the T cell's immune function that leads to T cell exhaustion making T cells ineffective (**Figure 3**).

However, monoclonal antibodies that target PD-1 and PD-L1 are being studied and used as these pathways are majorly taken by tumor cells to proliferate in host's body that are known to typically regulate activity of T cells for their own benefit that is to evade the immune responses generated against them. Accumulating evidences has suggested that by inhibiting the binding of PD-L1 to PD-1, the antitumor response is made stronger as the T cell exhaustion is reversed. Therefore, in view of that several monoclonal antibodies are being studied, particularly in TNBC like Atezolizumab, Avelumab and Durvalumab that specifically target PD-L1 and others such as Pembrolizumab and Nivolumab specific to target PD-1 [31].
