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. 2021 Jun 11;12:633361. doi: 10.3389/fimmu.2021.633361

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Copyright © 2021 Hu, Xu and Wei

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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Tumor infiltrates NK cells in hepatocellular carcinoma (HCC) and lung cancer. Left image: In the tumor microenvironment of lung cancer, NK cells up-regulated the expressions of CD69 and NKp44 and down-regulated the expression of NKp30, NKp80, DNAM-1 and CD16. Series of soluble molecules were secreted by tumor cells, like IDO, PGE2, and TGF-β. Tumor cells also could express membrane molecules that can shed receptors on the surface of NK cells. In addition, intratumoral NK cells showed impaired IFN-γ secretion, which may lead to inefficiency in DC maturation. Right image: In the tumor microenvironment of HCC, NK cells up-regulated KIR, NKG2A, PD1, TIM2, and CD96 inhibitory receptors while down-regulated NKG2D. Treg cells produced IL-10 and TGF-β. In HCC, TGFβ, prostaglandin E2 (PGE2) and indoleamine 2,3-dioxygenase (IDO), produced by tumor-associated fibroblasts inhibit the cytotoxic activity and cytokine secretion of NK cells.