Lymphocyte-activation gene 3 (LAG-3) as a promising immune checkpoint in cancer immunotherapy: From biology to the clinic.

In recent years, there have been notable advancements in the field of cancer immunotherapy, namely in the area of immune checkpoint inhibition. The Lymphocyte-activation gene 3 (LAG-3) has garnered attention as a potentially valuable focus of study in this particular field. The present study examines the biological aspects of LAG-3, its clinical consequences, and the potential therapeutic opportunities associated with its modulation. LAG-3, similar to CD4, has a regulatory role in modulating the immune system. The upregulation of this protein inside the neoplastic milieu hampers the immune system's ability to mount an effective response, hence enabling the evasion of cancer cells from immune surveillance. The LAG-3 protein interacts with ligands, inhibiting cytotoxic immune cells such as CD8 T cells and NK cells. The potential of LAG-3 inhibitors presents intriguing prospects. Integrating these medicines with established treatments like PD-1/PD-L1 or CTLA-4 inhibitors can broaden the range of available therapy choices and address resistance issues. The advent of personalized therapy is imminent, as evidenced by the utilization of predictive biomarkers such as LAG-3 expression to inform individualized therapeutic approaches. Additionally, inhibitors of LAG-3 exhibit promise in addressing immunological depletion and resistance by revitalizing T cells and producing durable immune responses. The realization of LAG-3's promise necessitates global collaboration and equal access. Multinational trials are expected to ascertain the efficacy of the intervention in various patient groups.