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

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

PROVIDER: PRJNA634115 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11819113.fastq.gz	Fastqsanger.gz
	SRR11819114.fastq.gz	Fastqsanger.gz
	SRR11819115.fastq.gz	Fastqsanger.gz
	SRR11819116.fastq.gz	Fastqsanger.gz

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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

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-α. 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 through their 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 significantly 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 directly bound to and 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, raising the interesting possibility that the inhibition of ZFP36L2 in iTregs could be a therapeutic strategy for autoimmune diseases.

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ZFP36L2 post-transcriptionally controls acute myeloid leukemia differentiation (ZFP36L2 eCLIP)

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ZFP36L2 post-transcriptionally controls acute myeloid leukemia differentiation (ZFP36L2 KO RNA-seq)

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Helios KO Tregs

Project description:Helios KO Tregs

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Influence of ATL-type Helios overexpression or WT-Helios/Ikaros knockdown on gene expression profile in Jurkat cells

Project description:It has been known that aberrant isoforms of Ikaros family ptoteins are expressed in malignant cells. We identified that PBMC of ATL (acute T-cell leukemia) patients expresses different patterns of Helios isoforms compared with normal PBMC. In order to investigate the biological impact of ATL-type Helios isoform, we conducted complehensive gene expression analyses in Jurkat cells overexpressing ATL-type Helios. Also, we investigated the influence of WT-Helios or WT-Ikaros knockdown on the gene expression profile and compared with that of the cells with ATL-type Helios overexpression. Total RNA samples from Jurkat cells were subjected to Cy-3 labeling followed by human whole genome gene expression microarray analyses.

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ZFP36L2 post-transcriptionally controls acute myeloid leukemia differentiation (ZFP36L2 eCLIP)

Project description:ZFP36L2 post-transcriptionally controls acute myeloid leukemia differentiation (ZFP36L2 eCLIP)

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ChIP-seq HELIOS (Ikzf2)

Project description:Here we addressed the genome-wide DNA binding profile of Helios transcription factor in early hematopoietic progenitor cells. We reported Helios DNA target sites by performing Chromatin Immuno-Precipitation (ChIP) assay on genomic DNA from the early hematopoietic progenitor cells line HPC7.

2021-08-13 | GSE149242 | GEO

Influence of ATL-type Helios overexpression or WT-Helios/Ikaros knockdown on gene expression profile in Jurkat cells

2013-03-31 | GSE41796 | GEO

Exiguobacterium sp. Helios

Project description:Exiguobacterium sp. Helios Assembly

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