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. 2023 May 19;14:1125874. doi: 10.3389/fimmu.2023.1125874

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Copyright © 2023 Kumar and Stewart

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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ILCs and NK cells in TIME and their immunometabolism. Different ILCs, including cytotoxic NK cells, are present in TME or TIME. The increased TGF-β levels in TIME transform high cytotoxic NK cells to less cytotoxic ILC1s and ILC3s to ILC3regs, which release IL-10 to support immunosuppressive TIME. Also, the high lactate levels in TIME or TME decrease NK cell OXPHOS, induce mitochondrial damage, and their apoptosis. Hence, the NK cell cytotoxicity (NKCC) is blocked in the immunosuppressive TIME that supports tumor growth. Furthermore, i-ILC2s polarize to n-ILC2s in the presence of TIME IL-25, further supporting angiogenesis, tumor growth, and metastasis by releasing immunosuppressive cytokines (IL-5 and IL-13). IL-5 and IL-13 are released from n-ILC2s in response to IL-33, increasing their OXPHOS and FAO. GM-CSF release from immature NK cells increases MDSCs proliferation, supporting immunosuppression. See text for details.