Abstract
Recent development of cancer immunotherapy, and CAR-T cell therapy in particular, attracts considerable attention among researchers. In antitumor immunity, cytotoxic T lymphocytes (CTLs) specifically recognize tumor-associated antigens (TAAs) in an MHC-class I-restricted manner and attack tumor cells. CTL activation and its clonal expansion require co-stimulatory receptors such as CD28, 4-1BB and OX40, and CTL stimulatory cytokine including IL-2 and IFNγ in addition to antigen recognition. However, tumor cells escape from the immune surveillance via decreased expression of MHC class 1, increased expression of co-inhibitory molecule, inhibitory cytokine production and accumulation of inhibitory immune cells during in vivo growth. CAR gene-designated extracellular binding domain consists of a target-specific antibody or a targeting ligand fused with the intracellular activating CD3zeta chain and the co-stimulatory molecule gene (1).
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