The programmed death receptor-1 (PD-1) functions as an immune checkpoint, limiting tissue damage and preventing the development of autoimmunity during inflammatory responses. It is primarily expressed on activated T cells and negatively modulates T cell effector functions by binding to its ligands.

One of the main ligands of PD-1 is PD-L1. PD-L1 expression in normal tissues is a major immune tolerance mechanism to control tissue autoimmune responses after a sustained inflammatory response due to tissue damage. However, tumor cells could also take advantage of the PD-1/PD-L1 junction as a molecular “shield” to attenuate T-cell-mediated cytotoxicity and thus evade immune surveillance.

Immunotherapy based on PD1 blockade to enhance antitumor immunity originated from observations in chronic infection models, where impairing PD1 interactions with its ligands reversed T-cell depletion. Blockade of PD1 prevents interaction with its ligand (PDL1) located on the cells of tumor cells, leading to the restoration of antitumor immunity mediated by T cells.

Currently there are different therapeutic antibodies specific to PD-1, however, its high cost has limited its use in Mexico, restricting its access to most of the population. The development of this antibody will allow establishing the platform for the generation of molecules with specificities against other antigens involved in other diseases.

The unit is currently developing a discovery campaign to obtain an anti-PD-1 antibody that binds with high affinity and specificity that effectively inhibits the interaction between PD-1 and its ligands through the phage display technique and the use of of semi-synthetic libraries of single chain variable fragments or scFv.