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Interleukin-35 impairs human NK cell effector functions and induces their ILC1-like conversion with tissue residency features

ABSTRACT: Interleukin-35 impairs human NK cell effector functions and induces their ILC1-like conversion with tissue residency features

PROVIDER: PRJNA1078317 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28024465.fastq.gz	Fastqsanger.gz
	SRR28024466.fastq.gz	Fastqsanger.gz
	SRR28024467.fastq.gz	Fastqsanger.gz
	SRR28024468.fastq.gz	Fastqsanger.gz
	SRR28024469.fastq.gz	Fastqsanger.gz

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Interleukin-35 impairs human NK cell effector functions and induces their ILC1-like conversion with tissue residency features

Project description:While Natural Killer (NK) cells are key players in immune defenses against pathogens and cancers, by directly killing dangerous cells and supporting antitumor functions of other immune cells, they progressively get dysfunctional in chronic inflammatory diseases through mechanisms that remain insufficiently understood. NK cell development, survival, activation, and functions are highly regulated by cytokines. Among them, Interleukin 35 (IL-35), a new member of the IL-12 family released during chronic inflammations, plays a role in immune suppression. However, the direct effect of IL-35 on NK cells is still unknown. In this study, we observed that IL-35-exposed human primary NK cells display dampened proliferation and effector functions associated with differential expressions of activating and inhibitory NK receptors. Brief exposure to IL-35 inhibited NK cell activation and ability to secrete pro-inflammatory cytokines and chemokines, while promoting their production of pro-angiogenic factors and TGF-β. Furthermore, prolonged exposure to IL-35 placed NK cells in a functionally hyporesponsive state associated with a TGF-β-dependent conversion into CD9+ CD103+ CD49a+ ILC1-like cells. Single cell RNAseq further confirmed these observations and revealed an ILC1-like heterogeneity associated to the initial NK subpopulation undergoing the conversion. Thus, our findings identify a new role of IL-35 as a driver of NK cell plasticity leading to the acquisition of tissue residency features and weakened effector functions that might play a role in physiopathological contexts and represent an attractive target for future immunotherapies.

2025-05-27 | GSE256137 | GEO

Toxoplasma gondii Infection Promotes NK Cell Conversion into ILC1s and Heterogeneous ILC1 Populations

Project description:Toxoplasma gondii Infection Promotes NK Cell Conversion into ILC1s and Heterogeneous ILC1 Populations

| PRJNA512527 | ENA

Gene expression analysis of CD4+ and CD4- ILC1 subsets by RNAseq

Project description:Innate lymphoid cell (ILC) subsets that mirror helper T cells in their effector cytokine profiles have recently emerged as central players in both homeostatic and inflammatory conditions. Like their Th1, Th2 and Th17/Th22 helper T cell counterparts, ILC subsets are categorized based on their expression of specific transcription factors and effector cytokines: group 1 ILC (ILC1) express T-bet and IFN-Î³; group 2 ILC (ILC2) express GATA-3 and type 2 effector cytokines such as IL-13 and IL-5; and group 3 ILC (ILC3) express RORgt and the cytokines IL-22 and/or IL-17. Under this nomenclature, natural killer (NK) cells and lymphoid tissue inducers (LTi) are considered ILC1 and ILC3, respectively. ILC1 contain both CD4+ and CD4- populations, but whether this phenotypic characteristic reflects functional differences between these two populations is unknown. These studies examine the gene expression profiles of CD4+ vs CD4- ILC1 in a cohort of healthy control subjects. ILC subsets were isolated from the peripheral blood of healthy control subjects. cDNA was isolated and amplified from sorted populations, and gene expression was analyzed by RNAseq

2015-12-31 | E-GEOD-69596 | biostudies-arrayexpress

SMAD4 impedes conversion of NK cells into ILC1-like cells by curtailing non-canonical TGFb signaling (mouse data sets)

Project description:Among the features that distinguish type 1 innate lymphoid cells (ILC1s) from NK cells is a gene signature indicative of TGFb-family cytokine imprinting. To assess the impact of TGFb family cytokines on ILC1 differentation, we examined SMAD4- a transcription factor that facilitates the signaling pathway common to all TGFb family cytokines-was specifically ablated in ILCs and NK cells. While SMAD4 deficiency did not affect ILC1 differentation, NK cells paradoxically aquired an ILC1-like gene signature and were incapable of controlling tumor metastasis and viral infection. We used microarray to define the transcriptional differences between splenic NK cells from WT and SMAD4F/F x Ncr1-Cre mice.

2017-07-31 | GSE100247 | GEO

SMAD4 impedes conversion of NK cells into ILC1-like cells by curtailing non-canonical TGFb signaling (human data sets)

Project description:Among the features that distinguish type 1 innate lymphoid cells (ILC1s) from NK cells is a gene signature indicative of TGFb-family cytokine imprinting. To assess the impact of TGFb family cytokines on ILC1 differentation, we examined SMAD4- a transcription factor that facilitates the signaling pathway common to all TGFb family cytokines-was specifically ablated in ILCs and NK cells. While SMAD4 deficiency did not affect ILC1 differentation, NK cells paradoxically aquired an ILC1-like gene signature and were incapable of controlling tumor metastasis and viral infection. We used microarray to compare the transcriptional differences between human blood NK cells. NK cells from a patient with a deleterious SMAD4 mutation or control NK cells were cultured overnight with either IL-2 alone or TGFb1 and IL-2.

2017-07-31 | GSE100246 | GEO

SMAD4 impedes conversion of NK cells into ILC1-like cells by curtailing non-canonical TGFb signaling

Project description:SMAD4 impedes conversion of NK cells into ILC1-like cells by curtailing non-canonical TGFb signaling

| PRJNA391153 | ENA

Effect of PDGF-Ddstimulation on human tonsil ILC1

Project description:The effect of PDGF-DD on the gene expression of human tonsil ILC1 is unknown. We used microarray to determine the transcriptional differences between unstimulated and PDGF-DD-stimulated human tonsil ILC1.

2018-02-01 | GSE107043 | GEO

mRNA-sequencing of ILC1 cells

Project description:Purpose: To understanding the effects of RORa deficiency on ILC1 cells, we conducted bulk mRNA-seqencing Method: Firstly, we purified liver ILC1 cells (CD45.2+CD3-CD19-NKp46+NK1.1+CD49a+CD49b-) via Fluorescence Activated Cell Sorting, then frozen in -80 °C ultra-low temperature refrigerator, followed by High-throughput sequencing, in three replicates for WT (Rorafl/fl) mice and one replicate for cKO (Ncr1Cre-Rorafl/fl) , using Illumina Hiseq 1500 platform.

2022-09-28 | GSE186193 | GEO

MCMV-experienced ILC1 acquire an m12-dependent memory response

Project description:Innate and adaptive immune cells can acquire “memory” of encounters with a diverse range of activating signals to tune their response to secondary stimuli. Group 1 innate lymphoid cells (ILC1) are recently discovered tissue-resident sentinels that are essential for early host protection from intracellular pathogens at initial sites of infection. However, whether ILC1 function as short-lived effectors or persist and refine their responsiveness following pathogen challenge is not well understood. Furthermore, whether pathogen-derived antigens directly modulate tissue-resident ILC responses remains unclear. Here, we found that liver-resident ILC1 expand locally and persist following the resolution of mouse cytomegalovirus (MCMV) infection. MCMVexperienced ILC1 acquired stable transcriptional, epigenetic, and phenotypic changes, with an enhanced protective effector response to secondary MCMV challenge. Protective memory ILC1 responses were dependent on the MCMV-encoded glycoprotein m12, but not formed during bystander cytokine activation following heterologous infection. Thus, liver ILC1 acquire adaptive features in a MCMV-specific manner.

2019-05-02 | GSE128906 | GEO

mRNA-sequencing of ILC1 cells

Project description:mRNA-sequencing of ILC1 cells

| PRJNA772937 | ENA