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Cholesterol metabolism drives regulatory B cell IL-10 through geranylgeranyl pyrophosphate

ABSTRACT: Cholesterol metabolism drives regulatory B cell IL-10 through geranylgeranyl pyrophosphate

PROVIDER: PRJNA631655 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11767757_1.fastq.gz	Fastqsanger.gz
	SRR11767757_2.fastq.gz	Fastqsanger.gz
	SRR11767758_1.fastq.gz	Fastqsanger.gz
	SRR11767758_2.fastq.gz	Fastqsanger.gz
	SRR11767759_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Cholesterol metabolism drives regulatory B cell IL-10 through geranylgeranyl pyrophosphate

Project description:Regulatory B cells restrict immune and inflammatory responses across a number of contexts. This capacity is mediated primarily through the production of IL-10. Here we demonstrate that the induction of a regulatory program in human B cells is dependent on a metabolic priming event driven by cholesterol metabolism. Synthesis of the metabolic intermediate geranylgeranyl pyrophosphate (GGPP) was required to specifically drive IL-10 production, and to attenuate Th1 responses. Furthermore, GGPP-dependent protein modifications controlled signaling through PI3Kd-AKT-GSK3, which in turn promoted BLIMP1-dependent IL-10 production. Inherited gene mutations in cholesterol metabolism result in a severe autoinflammatory syndrome, termed mevalonate kinase deficiency (MKD). Consistent with our findings, B cells from MKD patients induced poor IL-10 responses and were functionally impaired. Moreover, metabolic supplementation with GGPP was able to reverse this defect. Collectively, our data define cholesterol metabolism as an integral metabolic pathway for the optimal functioning of human IL-10 producing regulatory B cells.

2020-05-12 | GSE150245 | GEO

Cholesterol metabolism drives regulatory B cell IL-10 through provision of geranylgeranyl pyrophosphate.

Project description: Not available

| S-EPMC7343868 | biostudies-literature

IL-10

Project description:IL-10

| PRJNA1061148 | ENA

ICOS-driven Cholesterol and Cortisol Biosynthesis Shape IL-10 Production in ILC2s to Regulate Airway Hyperreactivity

Project description:Group 2 innate lymphoid cells (ILC2) induce type 2 inflammation in the lungs in response to allergens. Here, we investigated the regulatory mechanism of IL-10 production by ILC2s on the development of airway hyperreactivity (AHR), with a particular focus on the role of ICOS. Our findings demonstrate that inhibition of ICOS in pulmonary ILC2s significantly promotes IL-10 production. Lack of ICOS reprograms ILC2 steroid metabolism, resulting in increased cholesterol and cortisol biosynthesis and Glucocorticoid receptor (GR) activation. Consequently, this reprogramming regulates MAF and NFIL3 activation, thereby promoting IL-10 production. We notably found that in vivo GR inhibition or ILC2-specific GR deficiency exacerbated the development of AHR in multiple mouse models. Finally, we extended our findings to a human setting and demonstrated concordant results between murine models and human ILC2s. Taken together, our results therefore indicate that ICOS negatively regulates IL-10 production in ILC2s by controlling cholesterol and cortisol biosynthesis.

2025-06-24 | GSE288711 | GEO

IL-36/LXR axis modulates cholesterol metabolism and immune defense to Mycobacterium tuberculosis

Project description:Mycobacterium tuberculosis (Mtb) is a life-threatening pathogen in humans. Bacterial infection of macrophages usually triggers strong innate immune mechanisms, including IL-1 cytokine secretion. The newer member of the IL-1 family, IL-36, was recently shown to be involved in cellular defense against Mtb. To unveil the underlying mechanism of IL-36 induced antibacterial activity, we analyzed its role in the regulation of cholesterol metabolism, together with the involvement of Liver X Receptor (LXR) in this process. Here we report that, in Mtb-infected macrophages, IL-36 signaling modulates cholesterol biosynthesis and efflux via LXR. Moreover, IL-36 induces the expression of cholesterol-converting enzymes and the accumulation of LXR ligands, such as oxysterols. Ultimately, both IL-36 and LXR signaling play a role in the regulation of antimicrobial peptides expression and in Mtb growth restriction. These data provide novel evidence for the importance of IL‑36 and cholesterol metabolism mediated by LXR in cellular host defense against Mtb.

2018-02-14 | GSE103092 | GEO

CD8+ T cells: IL-10+ VS IL-10-

Project description:Transcriptional profiling and gene expression profiling analysis of sorted CD8+IL-10+ T cells compared to CD8+IL-10- T cells using IL-10-GFP(tiger) reporter mice

2013-06-21 | GSE37739 | GEO

Monocyte-derived IL-10 drives sex differences in pain duration

Project description:Women frequently experience longer-lasting pain than men, indicating delayed pain resolution. While we understand that pain can be orchestrated by the close interplay between the sensory nervous system and the immune system, it remains unclear whether this interaction contributes to the longer duration of pain in women. Here, we demonstrate that interleukin (IL)-10+ monocytes resolve inflammatory pain by signaling to IL-10R1+ sensory neurons in a mouse model of skin inflammation. A higher number of IL-10+ monocytes in males enables faster resolution of inflammatory pain compared to females. In both sexes, pain resolution was impaired by deleting Il10 from monocytes or Il10ra from sensory neurons. Similarly, in humans, men’s pain resolved faster than women’s after traumatic injury, which was associated with higher levels of circulating monocytes and IL-10 in men. In mice, androgen signaling promotes IL-10 production by monocytes, resulting in sex differences in the number of IL-10+ monocytes. Enhancing IL-10+ monocytes in the inflamed skin through Resolvin D1 treatment accelerated pain resolution in both sexes of mice. Our findings uncover a novel role for peripheral IL-10+ monocytes in driving sex differences in pain resolution. These results reveal a previously underappreciated contribution of immune cells to resolving pain and preventing the transition to chronic pain.

2026-01-14 | GSE316149 | GEO

Expression data from IL-10+ and IL-10- CD8 T cells

Project description:IL-10 is an anti-inflammatory cytokine that has been shown to be produced by antigen-specific CD8 T cells at the peak of viral encephalitis. We found that IL-10+CD8 T cells are more activated and cytolytic than IL-10-CD8 T cells. We used microarrays to detect gene expression changes in directly ex vivo sorted CNS IL-10+ and IL-10- CD8 T cells from a neurotropic J2.2-V-1-infected mouse.

2010-12-07 | GSE25846 | GEO

CD8+ T cells: IL-10+ VS IL-10-

Project description:Transcriptional profiling and gene expression profiling analysis of sorted CD8+IL-10+ T cells compared to CD8+IL-10- T cells using IL-10-GFP(tiger) reporter mice Two sample, CD8+IL-10+ T cells vs CD8+IL-10- T cells. Three replicate per array.

2013-06-21 | E-GEOD-37739 | biostudies-arrayexpress

IL-10+ T cells compared to IFNg+/IL-10- T cells induced by IL-10 tolerogenic dendritic cells

Project description:Ex vivo generated tolerogenic dendritic cells (tDCs) have a strong therapeutic potential to induce antigen-specific iTreg upon infusion in patients. We previously demonstrated that IL-10 tDC-primed T cells are very suppressive and produce IL-10. Here, we show that the majority of the IL-10+ T cells co-express IFNγ, giving rise to the question whether these cells are proinflammatory or regulatory. Whole genome gene expression analysis revealed a strong regulatory gene profile and a suppressed Th1 gene profile for the IL-10/ IFNγ co-expressing CD4+ T cells.

2015-07-03 | GSE70483 | GEO

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