先天淋巴细胞（ILCs）是一组先天淋巴细胞，它们不表达RAG依赖的改变的抗原特异性细胞表面受体。根据它们的发育轨迹和细胞因子产生基因型，ILCs被分为五组。它们包括NK细胞，它们是细胞毒性的，类似于CD4+ T辅助（Th）1-3的帮助样ILCs，以及淋巴组织诱导细胞（LTi）。NK细胞的发展取决于Eomes（eomesodermin），而ILC1计划主要由转录因子T-bet（T-box转录因子Tbx21）调节，ILC2的计划由GATA3（GATA结合蛋白3）调节，ILC3的计划由RORγt（RAR相关孤儿受体γ）调节。NK细胞是在近50年前发现的，但ILC1仅在大约15年前首次被描述。在ILC家族中，NK和ILC1具有许多相似之处，正如它们的细胞表面表型在很大程度上重叠所证实的那样。NK细胞和ILC1已被报告对组织炎症和细胞内病原体做出反应。许多研究已经报道了NK细胞在人类和小鼠中的抗肿瘤作用，但ILC1的数据既稀缺又矛盾。在本综述中，我们将首先描述不同的NK细胞和ILC1亚群、它们的效应细胞功能和发育。然后我们将讨论它们在癌症中的作用和肿瘤微环境对它们代谢的影响。Copyright © 2023 Elsevier Ltd. All rights reserved.

Innate lymphoid cells (ILCs) are a group of innate lymphocytes that do not express RAG-dependent rearranged antigen-specific cell surface receptors. ILCs are classified into five groups according to their developmental trajectory and cytokine production profile. They encompass NK cells, which are cytotoxic, helper-like ILCs 1-3, which functionally mirror CD4+ T helper (Th) type 1, Th2 and Th17 cells respectively, and lymphoid tissue inducer (LTi) cells. NK cell development depends on Eomes (eomesodermin), whereas the ILC1 program is regulated principally by the transcription factor T-bet (T-box transcription factor Tbx21), that of ILC2 is regulated by GATA3 (GATA-binding protein 3) and that of ILC3 is regulated by RORγt (RAR-related orphan receptor γ). NK cells were discovered close to fifty years ago, but ILC1s were first described only about fifteen years ago. Within the ILC family, NK and ILC1s share many similarities, as witnessed by their cell surface phenotype which largely overlap. NK cells and ILC1s have been reported to respond to tissue inflammation and intracellular pathogens. Several studies have reported an antitumorigenic role for NK cells in both humans and mice, but data for ILC1s are both scarce and contradictory. In this review, we will first describe the different NK cell and ILC1 subsets, their effector functions and development. We will then discuss their role in cancer and the effects of the tumor microenvironment on their metabolism.Copyright © 2023 Elsevier Ltd. All rights reserved.