Blockade of the checkpoint receptor TIGIT prevents NK cell exhaustion and elicits potent anti-tumor immunity

Journal: Nature Immunology

Published: 2018-06-18

DOI: 10.1038/s41590-018-0132-0

Affiliations: 6

Authors: 12

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Research Highlight

Targeting TIGIT

© JUAN GAERTNER/SCIENCE PHOTO LIBRARY/Getty

© JUAN GAERTNER/SCIENCE PHOTO LIBRARY/Getty

Blocking a protein called TIGIT doesn’t just unleash the anti-tumour activity of T cells, it also spurs natural killer (NK) cells — another type of immune cell — to attack cancer, according to a study led by researchers from the University of Science and Technology of China.

Working with mouse models of several forms of cancer, the researchers showed that inhibiting TIGIT, either genetically or with an antibody drug, impaired tumour growth. This effect depended on both T cells and NK cells.

Other checkpoint molecules — including PD-1 and CTLA-4, both targets of existing immunotherapy drugs — also neutralized T cell function, but only TIGIT expression impacted NK cells. Therapeutic targeting of TIGIT could benefit patients whose T cells who don’t respond to current immunotherapies but who may have NK cells that are still amenable to modulation. Combinatorial strategies may also improve clinical outcomes.

Supported content

  1. Nature Immunology 19, 723–732 (2018). doi: 10.1038/s41590-018-0132-0
Institutions FC
First Affiliated Hospital, AHMU, China 0.33
CAS Key Laboratory of Innate Immunity and Chronic Disease, USTC, China 0.26
Institute of Immunology, USTC, China 0.26
Hefei National Laboratory for Physical Sciences at the Microscale (HFNL), China 0.11
Shenzhen Laboratory of Fully Humanized Antibody Engineering, SIAT CAS, China 0.02
Institute of Biomedicine and Biotechnology (IBB), SIAT CAS, China 0.02

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