Journal
CANCER IMMUNOLOGY IMMUNOTHERAPY
Volume 65, Issue 3, Pages 305-314Publisher
SPRINGER
DOI: 10.1007/s00262-016-1799-4
Keywords
TIGIT; CD155; DNAM-1; CIK cells; Immunotherapy
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Funding
- National Natural Science Foundation of China [81202015]
- Jiangsu Provincial Special Program of Medical Science [BL2012020]
- Natural Science Foundation of the Jiangsu Province Higher Education Institutions [12KJB320014]
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T cell Ig and ITIM domain (TIGIT) is a newly identified inhibitory receptor expressed on T and natural killer (NK) cells. Cytokine-induced killer (CIK) cells express CD3 and CD56 molecules, and share functional properties with both NK and T cells. However, it remains unknown whether TIGIT is expressed in CIK cells. Here, we show that TIGIT is expressed by CIK cells and interacts with CD155. By blocking TIGIT using an anti-TIGIT functional antibody, we demonstrate that CIK cells display increased proliferation; higher cytotoxic targeting of tumor cells expressing CD155; and higher expression of interferon-gamma (IFN-gamma), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha). Furthermore, increases in IFN-gamma and cytotoxicity by blockade of TIGIT were reduced by blocking DNAX accessory molecule-1 (DNAM-1) signaling, implying that TIGIT exerts immunosuppressive effects by competing with DNAM-1 for the same ligand, CD155. Our results provide evidence that blockade of TIGIT may be a novel strategy to improve the cytotoxic activity of CIK cells.
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