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RNA squencing of human NK cells activated with IL-15, a combination of IL-12, IL-15, and IL-18, or with a trimeric fusion protein 18/12/TxM

ABSTRACT: Gene expression analysis of human NK cells at baseline, Day 1, and Day 6 after activation with IL-15, IL-12/15/18, or the 18/12/TxM molecule

ORGANISM(S): Homo sapiens

PROVIDER: GSE166268 | GEO | 2022/02/02

REPOSITORIES: GEO

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RNA squencing of human NK cells activated with IL-15 or IL-12, IL-15, and IL-18

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RNA squencing of human NK cells activated with IL-15, a combination of IL-12, IL-15, and IL-18, or with a trimeric fusion protein 18/12/TxM

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Transcriptional changes in IL-2, IL-12 and IL-18 stimulated human natural killer cells

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Effect of IL-12+IL-18 or anti-NK1.1 stimulation on splenic NK cells [mNK_Activation_RNA-seq]

Project description:We stimulated freshly enriched splenic NK cells with either IL-12+IL-18 (1ng/ml each) or plate-bound anti-NK1.1. NKs from several C57Bl/6 mice were pooled. We then performed gene expression profiling analysis using data obtained from RNA-seq at two time points: 3 or 6 hours.

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Glucocorticoids and the cytokines IL-12, IL-15 and IL-18 present in the tumor microenvironment induce PD-1 expression on human Natural Killer cells

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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Project description:We used Affymetrix expression arrays to determine changes in gene expression associated with activation of human NK cells mediated through treatment with cytokines IL-2, IL-12 and IL-18 over a 24 hour period. Human natural killer cells were isolated via negative selection from PBMCs of healthy donors. Cells were found to be > 95% CD3-CD56+. RNA was harvested at time of isolation or after 24 hour stimulation from 8 x 10^6 cells per condition. For stimulations, cells were incubated at 37C (5% CO2) in RPMI, suuplemented with 10% Fetal Bovine Serum at 1.5 x 10^6 cells/ml. Cytokine stimualtions were conducted with IL-2 (100U/mL), IL-12 (10ng/mL) and IL-18 (100ng/mL) from 2 male donors (N = 4). Expression analysis was carried out to determine transcriptional changes associated with 24 hr stimulation relative to freshly isolated cells.

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A novel fusion protein scaffold 18/12/TxM activates the IL-12, IL-15, and IL-18 receptors to induce human memory-like natural killer cells.

Project description:Natural killer (NK) cells are cytotoxic innate lymphoid cells that are emerging as a cellular immunotherapy for various malignancies. NK cells are particularly dependent on interleukin (IL)-15 for their survival, proliferation, and cytotoxic function. NK cells differentiate into memory-like cells with enhanced effector function after a brief activation with IL-12, IL-15, and IL-18. N-803 is an IL-15 superagonist composed of an IL-15 mutant (IL-15N72D) bound to the sushi domain of IL-15Rα fused to the Fc region of IgG1, which results in physiological trans-presentation of IL-15. Here, we describe the creation of a novel triple-cytokine fusion molecule, 18/12/TxM, using the N-803 scaffold fused to IL-18 via the IL-15N72D domain and linked to a heteromeric single-chain IL-12 p70 by the sushi domain of the IL-15Rα. This molecule displays trispecific cytokine activity through its binding and signaling through the individual cytokine receptors. Compared with activation with the individual cytokines, 18/12/TxM induces similar short-term activation and memory-like differentiation of NK cells on both the transcriptional and protein level and identical in vitro and in vivo anti-tumor activity. Thus, N-803 can be modified as a functional scaffold for the creation of cytokine immunotherapies with multiple receptor specificities to activate NK cells for adoptive cellular therapy.

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