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PPP2R2D suppresses interleukin-2 production and regulatory T cell function

ABSTRACT: PPP2R2D suppresses interleukin-2 production and regulatory T cell function

PROVIDER: PRJNA659522 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12522980_1.fastq.gz	Fastqsanger.gz
	SRR12522980_2.fastq.gz	Fastqsanger.gz
	SRR12522981_1.fastq.gz	Fastqsanger.gz
	SRR12522981_2.fastq.gz	Fastqsanger.gz
	SRR12522982_1.fastq.gz	Fastqsanger.gz

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PPP2R2D suppresses interleukin-2 production and regulatory T cell function

Project description:Upon ATAC-seq, we found that lack of PPP2R2D expression in Tconv cells boosts chromatin opening of a large number of genes, while in Treg cells chromatin remodeling is limited. These findings demonstrate that PPP2R2D is more important in the direct regulation of Tconv cell function (IL-2 production) rather than Treg cell function.

2020-08-27 | GSE156927 | GEO

Oxidative Phosphorylation Regulates Interleukin-10 Production in Regulatory B Cells via the Extracellular Signal-related Kinase Pathway

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RNA-binding Protein ZFP36L2 Downregulates Helios Expression and Suppresses the Function of Regulatory T Cells

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A function for interleukin 2 in Foxp3-expressing regulatory T cells

Project description:Regulatory T cells (Treg cells) expressing the forkhead family transcription factor Foxp3 are critical mediators of dominant immune tolerance to self. Most Treg cells constitutively express the high-affinity interleukin 2 (IL-2) receptor alpha-chain (CD25); however, the precise function of IL-2 in Treg cell biology has remained controversial. To directly assess the effect of IL-2 signaling on Treg cell development and function, we analyzed mice containing the Foxp3gfp knock-in allele that were genetically deficient in either IL-2 (Il2-/-) or CD25 (Il2ra-/-). We found that IL-2 signaling was dispensable for the induction of Foxp3 expression in thymocytes from these mice, which indicated that IL-2 signaling does not have a nonredundant function in the development of Treg cells. Unexpectedly, Il2-/- and Il2ra-/- Treg cells were fully able to suppress T cell proliferation in vitro. In contrast, Foxp3 was not expressed in thymocytes or peripheral T cells from Il2rg-/- mice. Gene expression analysis showed that IL-2 signaling was required for maintenance of the expression of genes involved in the regulation of cell growth and metabolism. Thus, IL-2 signaling seems to be critically required for maintaining the homeostasis and competitive fitness of Treg cells in vivo. Keywords: cell type comparison

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Proteasome Function is Required for Platelet Production

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Oxidative Phosphorylation Regulates Interleukin-10 Production in Regulatory B Cells via the Extracellular Signal-related Kinase Pathway

Project description:Regulatory B cells (Bregs) are immune cells that constrain the immune response and restrict inflammation via their expression of interleukin (IL)-10. However, the molecular mechanisms underlying Breg differentiation and IL-10 secretion remain unclear. Previous data suggest that cellular metabolism determines both the fate and function of these cells. Here, we suggest an essential role for mitochondrial oxidative phosphorylation (OXPHOS) in the regulation of IL-10 in these Bregs. We found that IL-10+ B cells from IL-10-green fluorescent protein-expressing mice had higher oxygen consumption rate than IL-10- B cells. In addition, inhibition of OXPHOS decreased the expression of IL-10 in B cells. Further, suppression of OXPHOS diminished the expression of surface markers for Bregs and impaired their therapeutic effects in dextran sulfate sodium-induced colitis. Mechanistically, mitochondrial OXPHOS was found to regulate the transcription factor HIF-1α through the extracellular signal-related kinase pathway. Taken together, this study reveals a strong correlation between mitochondrial OXPHOS and Breg phenotype/function, indicating OXPHOS as a therapeutic target in autoimmune diseases driven by Breg dysfunction.

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Hydrogen sulfide produced by the microbiota suppresses GLP-1 production

Project description:Hydrogen sulfide produced by the microbiota suppresses GLP-1 production

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RNA-binding Protein ZFP36L2 Downregulates Helios Expression and Suppresses the Function of Regulatory T Cells

Project description:The zinc finger protein 36-like 2, ZFP36L2, is a member of a small family of RNA-binding proteins composed by ZFP36 (also known as tristetraprolin, TTP), ZFP36L1 and ZFP36L2 in humans, with corresponding murine orthologs. These proteins bind to adenine uridine-rich element (ARE) in the 3’untranslated region of target messenger RNA and stimulate target degradation. ZFP36 functions as an anti-inflammatory modulator in murine models of inflammatory diseases by down-regulating the production of inflammatory cytokines such as tumor necrosis factor-alpha. However, how ZFP36L1 and ZFP36L2 alter the function of CD4+ T cells is not completely understood. We addressed this issue by searching for the target genes of ZFP36L2 by comprehensive transcriptome analysis. We observed that ZFP36L2 is highly expressed in naïve CD4+ T cells; however, when CD4+ T cells are stimulated with T cell receptors, ZFP36L2 expression is rapidly reduced in both humans and mice. Among CD4+ T cell populations, the expression levels of ZFP36L2 in regulatory T cells (Tregs) were lower than those in naïve or effector CD4+ T cells. RNA-sequence analysis revealed that the forced expression of ZFP36L2 decreased Ikzf2 (encoding Helios) expression in Foxp3+ Tregs and inhibited the ability of induced Tregs (iTregs). ZFP36L2 destabilized the 3’untranslated region of Ikzf2 mRNA, which contains AU-rich elements. These results indicate that ZFP36L2 reduces the expression of Ikzf2 and suppresses iTreg function, suggesting that the inhibition of ZFP36L2 in iTregs could be a therapeutic strategy for autoimmune diseases.

2020-05-21 | GSE150937 | GEO

Excitatory Neuron-Derived Interleukin-34 Controls Cortical Developmental Microglia Function

Project description:Excitatory Neuron-Derived Interleukin-34 Controls Cortical Developmental Microglia Function

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