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RNA-sequencing of wild-type and IRF4-deficient splenic cDC2s

ABSTRACT: RNA-sequencing of wild-type and IRF4-deficient splenic cDC2s

PROVIDER: PRJNA780492 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16947386.fastq.gz	Fastqsanger.gz
	SRR16947387.fastq.gz	Fastqsanger.gz
	SRR16947388.fastq.gz	Fastqsanger.gz
	SRR16947389.fastq.gz	Fastqsanger.gz
	SRR16947390.fastq.gz	Fastqsanger.gz

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RNA-sequencing of wild-type and IRF4-deficient splenic cDC2s

Project description:We analyzed the transcriptome differences of wild-type and IRF4-deficient (CD11c-cre x Irf4fl/fl) type-2 conventional dendritic cells (cDC2s) in spleen. Wild-type or IRF4-deficient (CD11c-cre x Irf4fl/fl) bone marrow cells were transferred into lethal irradiated CD45.1 mice. 8 weeks later, splenic cDC2s were purified and prepared for RNA-seq analysis. Three technical repeats of ~10^5 cells per sample from each of one mouse were included. CD97 was downregulated in IRF4-deficient cDC2s. GSEA showed that upregulated and downregulated genes in CD97-deficient cells were strongly enriched in IRF4-regulated genes. These data are in accord with CD97 acting within the IRF4 gene-expression network.

2022-03-23 | GSE188832 | GEO

RNA-sequencing of wild-type and ArhGEF1-deficient splenic cDC2s

Project description:We analyzed the transcriptome differences of wild-type and ArhGEF1-deficient (Arhgef1-/-) type-2 conventional dendritic cells (cDC2s) in spleen. Wild-type or ArhGEF1-deficient (Arhgef1-/-) bone marrow cells were transferred into lethal irradiated CD45.1 mice. 8 weeks later, splenic cDC2s were purified and prepared for RNA-seq analysis. The gene expression profiles of CD97-, Gα13- and ArhGEF1-deficient cDC2s were highly similar, providing evidence that these molecules function in the same pathway.

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RNA-sequencing of wild-type, CD97- and Gα13-deficient splenic cDC2s

Project description:We analyzed the transcriptome differences of wild-type, CD97- and Gα13-deficient (Adgre5-/- and CD11c-cre x Gna13fl/fl) type-2 conventional dendritic cells (cDC2s) in spleen. Three technical repeats of ~10^5 cells per sample from each of one mouse were included. Compared to wild-type cDC2s, CD97- and Gα13-deficient cDC2s differentially expressed many genes, but CD97- and Gα13-deficient cDC2s were almost the same. GSEA showed that Mrtf-a dependent genes were upregulated in CD97- and Gα13-deficient cDC2s, which code for cytoskeleton proteins. These data support that CD97-Gα13 signaling regulates splenic cDC2 motility by the actin cytoskeleton.

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RNA-sequencing of wild-type and ArhGEF1-deficient splenic cDC2s

Project description:RNA-sequencing of wild-type and ArhGEF1-deficient splenic cDC2s

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RNA-sequencing of wild-type, CD97- and Gα13-deficient splenic cDC2s

Project description:RNA-sequencing of wild-type, CD97- and Gα13-deficient splenic cDC2s

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Transcription profiling by array of mouse irf4 knockout mature splenic B cells against wild type controls from littermates

Project description:Gene expression profiling of murine irf4-/- and irf4+/+ splenic B cells identifies genes regulated by the transcription factor IRF4 in quiescent mature B cells. B cells from 12-week old irf4-/- and irf4+/+ littermate mice were isolated by magnetic depletion of non-B cells from splenic mononuclear cells. RNA was isolated. Labeled cRNA was hybridized to microarrays and genes specifically expressed in irf4-/- vs. irf4+/+ samples.

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TGF-β promotes the conversion of human CD5low cDC2s to tolerogenic CD5high cDC2s

Project description:Human blood CD1c+ cDC2s can be divided into two functionally distinct subpopulations according to their CD5 expression. CD5high and CD5low cDC2s differ significantly in their gene expression, cytokine production, antigen presentation, and T cell polarization. However, the plasticity of CD5high and CD5low cDC2s was unknown. We found that about 40% CD5low cDC2s upregulated their CD5 expression when cultured in the presence of TGF-β. Transcriptome analysis revealed that the converted CD5high cDC2s are closer to cultured CD5high cDC2s, separating form unconverted CD5low cDC2s. Converted CD5high cDC2s with higher IRF4 upregulated some steady-state DC mature molecules, such CCR7, CD86, PD-L1 and CCL22. Unconverted CD5low cDC2s with higher MAFB upregulated some monocyte signature genes, such CCR2, CSF1R and CCL2. Moreover, Converted CD5high and unconverted CD5low cDC2s were significantly different in inducing CD4+ T cell polarization. Specifically, converted CD5high cDC2s recruited and induced more Treg cells than unconverted CD5low cDC2s. We also found that the ratio of CD5high cDC2s are significantly higher in colorectal tumor tissue comparing with paired paratumor tissue. In summary, TGF-β can effectively promote the conversion from CD5low cDC2s to CD5high cDC2s accompanied by phenotype and function change. This may be another mechanism which contributes to TGF-β induced immune suppression.

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Expression data from murine irf4-/- and irf4+/+ mature B cells purified by magnetic cell separation

Project description:Gene expression profiling of murine irf4-/- and irf4+/+ splenic B cells identifies genes regulated by the transcription factor IRF4 in quiescent mature B cells.

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Expression data from murine irf4-/- and irf4+/+ mature B cells purified by magnetic cell separation and stimulated with anti-CD40 antibodies and IL-4

Project description:Gene expression profiling of murine irf4-/- and irf4+/+ splenic B cells identifies genes regulated by the transcription factor IRF4 in CD40+IL-4 activated mature B cells. B cells from 12-week old irf4-/- and irf4+/+ littermate mice were isolated by magnetic depletion of non-B cells from splenic mononuclear cells and cultures with mitogens in vitro. RNA was isolated. Labeled cRNA was hybridized to microarrays and genes specifically expressed in irf4-/- vs. irf4+/+ samples.

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