Purpose: Innate lymphoid cells (ILCs) play essential roles in mucosal innate immunity. The presence and function of ILCs in human lung cancer have not been extensively studied. This study aimed to identify and analyze the characteristics of the predominant subgroups in lung cancer.
Methods: Single-cell suspensions were obtained from lung tissue diseased regions, non-diseased regions, and peripheral blood. The distribution of the ILC subgroups was analyzed by flow cytometry. The RNA of all samples was sequenced by BGI Group. Differentially expressed genes (DEGs) were assessed by functional and pathway enrichment analyses.
Results: ILC3s were exclusively increased in the lung cancer diseased region. The NKp44 + ILC3 subgroup was found in the diseased and non-diseased regions, but not in the peripheral blood. RNA sequencing indicated similar basic transcripts in NKp44 − ILC3s and NKp44 + ILC3s, but more enrichment in the signal transduction pathway and signaling molecules and interaction pathway in NKp44 + ILC3s. Compared with in NKp44 − ILC3s, gene transcripts tended to be upregulated in NKp44 + ILC3s in the Ras, RAP1, Jak-STAT, Notch, NF-κB, and Toll-like receptor signaling pathways and downregulated in the TGF-β signaling pathway. In the signaling molecules and interaction pathway, levels of most key molecules were higher in NKp44 + ILC3s in the cell adhesion molecules and cytokine-cytokine receptor interaction pathways.
Conclusion: ILC3s was the dominant group in lung cancer and NKp44 + ILC3s was significant in diseased region. By transcripts analysis, the upregulated pathways in NKp44 + ILC3s enable survival, proliferation, activation, interleukin production, and antigen presentation. Our results provide the transcript landscape of DEGs in NKp44 + and NKp44 − ILC3s in lung cancer, providing a theoretical basis for further study of potential therapies.