Pdcd1lg2, also known as PD-L2 or CD273, encodes a ligand for the programmed death receptor 1 (PD-1). The engagement of PD-1 by PD-L2 can inhibit T cell receptor-mediated proliferation and cytokine production by CD4+ T cells, leading to cell cycle arrest in G0/G1 [4]. This indicates its crucial role in regulating T cell responses and immune tolerance.

In colorectal cancer, tumor Pdcd1lg2 expression was inversely associated with Crohn-like lymphoid reaction, suggesting that Pdcd1lg2-expressing tumor cells may inhibit the development of tertiary lymphoid tissues during carcinogenesis [1]. In hepatocellular carcinoma, elevated expression of Pdcd1lg2 was associated with favorable recurrence-free survival, progression-free survival, disease-specific survival, and overall survival, and was related to immune infiltration [2]. In pan-cancer studies, Pdcd1lg2 not only impacted patient prognosis but was associated with clinical characteristics in some cancer types, and was correlated with immune cells and various immunosuppressive biomarkers, as well as mismatch repair, tumor mutation burden, microsatellite instability, and DNA methylation [3].

In conclusion, Pdcd1lg2 is a significant immune-regulating gene that plays a role in T cell response regulation. Its expression has implications in multiple cancers, influencing prognosis, immune cell infiltration, and immunosuppressive biomarker associations. Research on Pdcd1lg2 provides insights into cancer immunity and tumor development mechanisms, which may contribute to the development of more effective cancer treatment strategies.