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Gene expression profile at single cell level of tumor-infiltrating NK (tuNK) from CT26_b2m-/- tumor received IL-21 treatment or IL-21 and IL-15 combination treatment.

ABSTRACT: NK cells are considered as dominant killing while tumor cells downregulating MHC-I expression to avoid recognition, but NK cell function are impaired in the tumor microenvironment. We used single cell RNA sequencing to analyze the NK cell performance in tumor with IL-21 treatment.

ORGANISM(S): Mus musculus

PROVIDER: GSE282121 | GEO | 2025/11/20

REPOSITORIES: GEO

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Gene expression profile at single cell level of tumor-infiltrating NK (tuNK) from CT26_b2m-/- tumor received IL-21 treatment or IL-21 and IL-15 combination treatment.

Project description:Gene expression profile at single cell level of tumor-infiltrating NK (tuNK) from CT26_b2m-/- tumor received IL-21 treatment or IL-21 and IL-15 combination treatment.

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Project description:Background: PD-1 immune checkpoint blockade has provided significant clinical efficacy across various types of cancer by unleashing both T- and NK cell-mediated anti-tumor responses. However, resistance to immunotherapy occurs for many patients, rendering the identification of the mechanisms that control PD-1 expression extremely important to increase the response to the therapy Objective: To identify the stimuli and the molecular mechanisms that induce the de novo PD-1 expression on human NK cells in the tumor setting Methods: NK cells freshly isolated from peripheral blood of healthy donors were stimulated with different combinations of molecules, and PD-1 expression was studied at the mRNA and protein level. Moreover, ex vivo analysis of tumor microenvironment and NK cell phenotype was performed. Results: Glucocorticoids (GCs) are indispensable for PD-1 induction on human NK cells, in cooperation with a combination of cytokines that are abundant at the tumor site. Mechanistically, GCs together with IL-12, IL-15 and IL-18 not only upregulate PDCD1 transcription, but also activate a previously unrecognized transcriptional program leading to enhanced mRNA translation and resulting in an increased PD-1 protein amount in NK cells. Conclusion: Our results provide evidence of a novel immune suppressive mechanism of GCs involving the transcriptional and translational control of an important immune checkpoint

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