Figure 2.

Anti-PD-1 combined with other cells inhibiting tumor growth and metastasis. The addition of anti-PD1 to TILs increased RANKL expression, and anti-RANKL directly reduced PD-L1 expression on the non-lymphoid component tumor microenvironment. Therefore, the addition of RANKL blocker can improve the efficacy of PD1, CTLA4 and RANKL inhibitors, and increase the proportion of IFNγ and TNFα in tumor-infiltrating CD4⁺ and CD8⁺ T cells. In addition, CD28 on T cells binds to ligands on DC cells to regulate tumor cells. T cells were activation of co-stimulatory molecules by 4-1BB and 4-1BBL enhances the survival of primary T cell responses and memory T cells. Besides, anti-PD-1 significantly inhibits tumor growth by activating DCs to present tumor-associated antigens to primary T cells. When CIK is activated by binding of the antigen-antibody complex to the FcR, toxic particles are excreted to the cells, and binding of FasL and Fas, the tumor cells undergo apoptosis. In addition to the release of toxic particles and Fas/FasL, CD16 expressed on the surface of NK cells binds to antibodies and kills tumor cells.