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Updated: Oct 11, 2025
Isolation of Group 2 Innate Lymphoid Cells from Mouse Nasal Mucosa to Detect the Expression of CD226
Published on: May 10, 2022
Type 1 Innate Lymphoid Cells Limit the Antitumoral Immune Response
Margaux Vienne1, Marion Etiennot1, Bertrand Escalière1
1Aix-Marseille Univ, Centre National de la Recherche Scientifique (CNRS), Institut National de la Santé et de la Recherche Médicale (INSERM), Centre d'Immunologie de Marseille-Luminy (CIML), Marseille, France.
Abstract:
Natural killer (NK) cells are known to be able to kill established tumor cell lines, but important caveats remain regarding their roles in the detection and elimination of developing primary tumors. Using a genetic model of selective ILC1 and NK cell deficiency, we showed that these cells were dispensable for tumor immunosurveillance and immunoediting in the MCA-induced carcinogenesis model. However, we were able to generate primary cell lines derived from MCA-induced tumors with graded sensitivity to NK1.1+ cells (including NK cells and ILC1). This differential sensitivity was associated neither with a modulation of intratumoral NK cell frequency, nor the capacity of tumor cells to activate NK cells. Instead, ILC1 infiltration into the tumor was found to be a critical determinant of NK1.1+ cell-dependent tumor growth. Finally, bulk tumor RNAseq analysis identified a gene expression signature associated with tumor sensitivity to NK1.1+ cells. ILC1 therefore appear to play an active role in inhibiting the antitumoral immune response, prompting to evaluate the differential tumor infiltration of ILC1 and NK cells in patients to optimize the harnessing of immunity in cancer therapies.
Insights
Innate lymphoid cells type 1 (ILC1) and natural killer (NK) cells do not prevent primary tumor development. However, ILC1 infiltration into tumors critically influences tumor growth, suggesting a role in suppressing anti-tumor immunity.
Area of Science:
- Immunology
- Cancer Biology
- Cellular Immunology
Background:
- Natural killer (NK) cells are recognized for their cytotoxic functions against established tumors.
- The role of NK cells and innate lymphoid cells type 1 (ILC1) in the early detection and elimination of developing primary tumors remains less understood.
- Existing research has not fully elucidated the mechanisms by which these cells influence tumor immunosurveillance and immunoediting.
Purpose of the Study:
- To investigate the role of ILC1 and NK cells in tumor immunosurveillance and immunoediting during carcinogenesis.
- To determine the factors influencing tumor cell sensitivity to NK1.1+ cells, including NK cells and ILC1.
- To identify potential therapeutic targets by understanding the interplay between ILC1, NK cells, and tumor growth.
Main Methods:
- Utilized a genetic model for selective ILC1 and NK cell deficiency in a chemically induced carcinogenesis model.
- Generated primary tumor cell lines with varying sensitivities to NK1.1+ cells.
- Analyzed intratumoral immune cell frequencies and tumor cell activation capacity.
- Assessed ILC1 infiltration as a determinant of tumor growth.
- Performed bulk tumor RNA sequencing to identify gene expression signatures.
Main Results:
- ILC1 and NK cells were found to be dispensable for immunosurveillance and immunoediting in the MCA-induced carcinogenesis model.
- Generated tumor cell lines exhibited differential sensitivity to NK1.1+ cells, independent of NK cell frequency or tumor cell activation potential.
- ILC1 infiltration into the tumor microenvironment was identified as a critical factor in NK1.1+-dependent tumor growth.
- A specific gene expression signature correlated with tumor sensitivity to NK1.1+ cells.
Conclusions:
- ILC1 appear to play an active role in inhibiting anti-tumor immune responses, rather than directly eliminating developing tumors.
- Tumor sensitivity to NK1.1+ cells is significantly influenced by ILC1 infiltration.
- Evaluating differential ILC1 and NK cell infiltration in human cancers may offer strategies for optimizing immunotherapies.
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