ArticleNPJ precision oncology2026
Innate lymphoid cell heterogeneity and etiology-specific reprogramming in hepatocellular carcinoma.
Article in NPJ precision oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Hepatocellular carcinoma (HCC), the third leading cause of cancer-related deaths worldwide, arises from diverse etiologies that shape the tumor immune landscape, including the composition and function of innate lymphoid cells (ILCs). In this study, we integrated scRNA-seq, bulk RNA-seq, and CyTOF to profile ILCs from tumor and adjacent non-tumor liver tissues of 50 HCC patients with different etiologies (hepatitis B viral, HBV and non-viral, NV). ScRNA-seq revealed heterogenous ILC and NK clusters in non-tumor and tumor tissues. Notably, ILC1 could be subdivided into proliferative (ILC1p) and cytotoxic (ILC1c) phenotypes. ILC2 displayed classic type-2 immune traits with phenotypic heterogeneity, while ILC3 expressed key transcription factors and IL18. ILC subsets diverged significantly by disease etiology. In NV-HCC, ILC2s exhibited a pro-fibrotic and tumor-promoting signature with elevated IL13, TGFB1, and AREG expression. ILC1s in NV-HCC showed activated and cytotoxic phenotypes, whereas in HBV-HCC, they showed signs of exhaustion with increased CD96 and TIGIT. ILC1 from NV-HCC also displayed enhanced IL-2/IL-15 signaling and interactions with CD8 + T cells via HLA-E, suggestive of potential antitumor crosstalk. While our single-cell cohort size was limited, necessitating validation in larger datasets, our study reveals etiology-associated differences in ILC phenotypes in HCC and provides insight into their potential roles in modulating immune responses within the tumor microenvironment.
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