Figure 1.

Mechanisms of CIK cell anti-tumor activity. The majority of CIK cell cytotoxicity is exerted through the interaction between NKG2D and its ligand MIC A/B and ULPB 1–4, resulting in granule exocytosis and secretion of cytokines like IFN-γ. NK-like structures, such as DNAM-1, is also involved in the recognition and killing of tumor targets. Besides, CIK cells can eradicate tumors in an MHC-restricted manner by TCR engagement, which is the so-called “dual-functional capability”. CIK cell, cytokine induced killer cells; NKG2D, natural killer group 2 member D; MIC A/B, MHC class I polypeptide-related sequence A/B; ULPB 1–4, UL16 binding protein 1–4. DNAM-1, DNAX accessory molecule-1; TCR, T-cell receptor; MHC 1, major histocompatibility complex 1; IFN-γ, interferon-γ.