CROSSLINKING A MONOCLONAL ANTIBODY TO NKR- P2/NKG2D ON DENDRITIC CELLS INDUCES THEIR ACTIVATION AND MATURATION LEADING TO ENHANCED ANTITUMOR IMMUNE RESPONSE

摘要

Monoclonal antibody mediated therapy is a promising area of anticancer research. Agonistic monoclonal enhances immune responses to suppress cancer growth by stimulating specific receptor on immune cells. NKR-P2/NKG2D is the chief tumor recognition receptor of NK cells and some T cells, which recognizes stress inducible ligands on tumors and mediates immune cell activation. We have recently reported involvement of NKR-P2 in dendritic cell activation. We show the potential of agonistic anti-NKRP2 mAb (1A6), which mimics the NKR-P2 ligand and induces activation and maturation of DCs. Interaction of DCs with 1A6, enhances NO mediated apoptosis in tumor cells. Crosslinking of NKR-P2 with mAblA6 upregulates MHC-II, CD86, CD la, antigen presentation function, and decreases endocytic activity of DC, thus drives DCs to play a pivotal role in adaptive immune responses.