Maddineni Sainiteesh, Sharma Krishna, Mohammad Imran A, Shin June H, Sunwoo John B
Department of Otolaryngology-Head & Neck Surgery, Stanford University School of Medicine, Stanford, California, USA.
Otolaryngol Head Neck Surg. 2025 Feb;172(2):697-701. doi: 10.1002/ohn.1096. Epub 2024 Dec 25.
Intraepithelial type 1 innate lymphoid cells (ieILC1s) are tissue-resident lymphocytes in the microenvironment of head and neck squamous cell carcinoma. Here, we evaluate how these cells influence T-cell trafficking to tumors. We generated cytotoxic ieILC1-like cells from natural killer (NK) cells in vitro. Using an in vivo tumor model, we show that intratumoral ieILC1-like NK cells induce greater T cell trafficking into the tumor. Co-culture of ieILC1-like NK cells with the tumor cells resulted in elevated CXCL10 in the supernatant. Flow cytometry demonstrated that ieILC1-like NK cells produce robust amounts of IFNy, a known CXCL10 inducer, while CXCL10 was produced by tumor cells. These results indicate ieILC1-like NK cells induce tumor production of CXCL10, a proinflammatory chemokine that promotes T cell infiltration into the TME. The role of ieILC1-like NK cells in modulating clinical responses to immune checkpoint blockade warrants investigation.
上皮内1型固有淋巴细胞（ieILC1s）是头颈部鳞状细胞癌微环境中的组织驻留淋巴细胞。在此，我们评估这些细胞如何影响T细胞向肿瘤的迁移。我们在体外从自然杀伤（NK）细胞生成了细胞毒性ieILC1样细胞。使用体内肿瘤模型，我们发现肿瘤内ieILC1样NK细胞可诱导更多T细胞迁移至肿瘤。ieILC1样NK细胞与肿瘤细胞共培养导致上清液中CXCL10水平升高。流式细胞术表明，ieILC1样NK细胞产生大量已知的CXCL10诱导剂IFNγ，而CXCL10由肿瘤细胞产生。这些结果表明，ieILC1样NK细胞诱导肿瘤产生CXCL10，这是一种促炎趋化因子，可促进T细胞浸润至肿瘤微环境（TME）。ieILC1样NK细胞在调节免疫检查点阻断临床反应中的作用值得研究。
