Fig. 1

Antitumor effects of γδT cells. γδT cells inhibit tumor growth through receptor-ligand interactions. MHC class I-related chains A/B (MICA/B) and UL16-binding protein (ULBP) are upregulated in cancer cells and are recognized by natural killer, group 2, member D (NKG2D), which exerts cytotoxic effects in cooperation with γδTCR. DNAX accessory molecule-1 (DNAM-1) and nectin-like-5 have been proven to interact on Vδ2Vγ9T cells in hepatocellular carcinoma. Natural cytotoxicity receptors (NCRs), especially NKp46, which is negatively correlated with the risk of metastasis in colorectal cancer, are abundantly expressed on Vδ1T cells. The ligand for NKp30 on Vδ1T cells is B7-H6, which is common in lymphoma and leukemia. Tumor surface protein: hMSH2, F1-ATPase-related structure and annexin A2 could constitute danger signals for γδT cells recognition, reducing the possibility of immune shielding. Like natural killer cells, γδT cells kill cancer cells indirectly by releasing interferon-gamma (IFN-γ), thereby exhibiting a Th1 cell-like phenotype, or directly via the death receptor signal factor associated suicide ligand (FasL) and TNF-related apoptosis-inducing ligand (TRAIL), secreting cytotoxic molecules such as granzyme and perforin