(2018) show B7S1-B7S1R signaling additionally regulates CD8<sup>+</sup> T cell responses by working with the PD1-PDL1 checkpoint to block anti-tumor immunity.
In addition, depletion of B7-H4 could help restore CD8<sup>+</sup> T anti-tumor immunity by elevating the expression and secretion levels of CD107a, granzyme A, granzyme B, perforin and IFN-γ.
Our study provides for the first time evidence of B7-H4 expression on melanoma cells as a mechanism controlling tumor immunity which is associated with patients' survival.
Our results indicate a tight regulation of B7-H4 expression in the translational level in normal peripheral tissues and a potential role of B7-H4 in the evasion of tumor immunity.