Programmed cell death protein 1 (PD-1) (PD-1)

Programmed cell death protein 1 (PD-1) is a type I transmembrane protein and a member of the immunoglobulin superfamily that functions as a critical inhibitory checkpoint receptor [1]. Primarily expressed on the surface of activated T cells, B cells, and myeloid cells, PD-1 plays a vital role in maintaining peripheral tolerance and preventing autoimmunity by dampening T cell activity [2]. In the context of oncology, many tumors exploit the PD-1 pathway by expressing its ligands, PD-L1 and PD-L2, which bind to PD-1 on tumor-infiltrating CD8+ T cells to induce a state of exhaustion or anergy [3]. This interaction effectively shields the tumor from immune-mediated destruction [4]. Therapeutic intervention with anti-PD-1 monoclonal antibodies, such as pembrolizumab and nivolumab, disrupts this inhibitory signaling, thereby reinvigorating the cytotoxic potential of CD8+ T cells against malignant cells [2, 5]. While highly effective across multiple cancer types, PD-1 blockade can also trigger immune-related adverse events (irAEs) by disrupting the balance of immune regulation in healthy tissues [6].

Other names

PDCD1CD279Protein PD-1hPD-1SLEB2

PD-1 inhibitors are monoclonal antibodies that bind to the PD-1 receptor on T cells, blocking its interaction with PD-L1 and PD-L2 ligands [2]. This blockade prevents the inhibitory signal that normally suppresses T cell activation, thereby enhancing the immune system's ability to recognize and destroy cancer cells [4].