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. 2021 Jul 22;12:699895. doi: 10.3389/fimmu.2021.699895

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Copyright © 2021 Ge, Peppelenbosch, Sprengers and Kwekkeboom

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Blockade of TIGIT on NK cells augments anti-tumor immunity. (A) NK cells expressing TIGIT are functionally impaired by binding to CD155 and nectin-4, and in colorectal cancer to Fap2 protein produced by a gut bacterium. (B) TIGIT blockade not only interrupts inhibitory signaling by TIGIT in NK cells, but also allows interaction of the co-stimulatory receptor CD226 with CD155. IL-15 treatment increases TIGIT and CD226 expression on NK cells. Thus IL-15 combined with TIGIT blockade further enhanced NK cells anti-tumor functions, especially promoting NK cell-mediated destruction of MHC class I-deficient tumors.