CD2-CD58 interactions stabilize contact between immune cells and target cells and participate in the organization of T-cell and NK-cell immune synapses, amplification of activation signals, and maintenance of effector functions. Loss of CD58 or insufficient CD2 signaling can weaken antitumor ...
Tumor immune killing depends not only on whether immune cells are present, but also on the balance between inhibitory and activating signals. NKG2A restricts NK cell and CD8⁺ T cell function through HLA-E, whereas NKG2D recognizes tumor stress ligands and enhances immune killing. Together, these ...