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E-GEOD-53145

ABSTRACT: The transcriptional repressor BLIMP1 curbs host-defenses by suppressing expression of the chemokine CCL8

OTHER RELATED OMICS DATASETS IN: PRJNA231003

PROVIDER: E-GEOD-53145 | ExpressionAtlas | 2015-07-31

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-GEOD-53145-analysis-methods.tsv	Tabular
	E-GEOD-53145-atlasExperimentSummary.Rdata	Rdata
	E-GEOD-53145-configuration.xml	Xml
	E-GEOD-53145-percentile-ranks.tsv	Tabular
	E-GEOD-53145.condensed-sdrf.tsv	Tabular

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Mus musculus

Project description:The transcriptional repressor BLIMP1 curbs host-defenses by suppressing expression of the chemokine CCL8

| PRJNA231003 | ENA

The transcriptional repressor BLIMP1 curbs host-defenses by suppressing expression of the chemokine CCL8

Project description:The transcriptional repressor BLIMP1 is a master regulator of B and T cell differentiation. To examine the role of BLIMP1 in innate immunity we used a conditional knockout (CKO) of Blimp1 in myeloid cells and found that Blimp1 CKO mice were protected from lethal infection induced by Listeria monocytogenes. Transcriptome analysis of Blimp1 CKO macrophages identified the murine chemokine (C-C motif) ligand 8, CCL8 as a direct target of Blimp1-mediated transcriptional repression in these cells. BLIMP1-deficient macrophages expressed elevated levels of Ccl8 and consequently Blimp1 CKO mice had higher levels of circulating CCL8 resulting in increased neutrophils in the peripheral blood, promoting a more aggressive anti-bacterial response. Mice lacking the Ccl8 gene were more susceptible to L. monocytogenes infection than wild type mice. While CCL8 failed to recruit neutrophils directly, it was chemotactic for Î³/Î´ T cells and CCL8-responsive Î³/Î´ T cells were enriched for IL-17F. Finally, CCL8-mediated enhanced clearance of L. monocytogenes was dependent on Î³/Î´ T cells. Collectively, these data reveal an important role for BLIMP1 in modulating host-defenses by suppressing expression of the chemokine CCL8. RNA (5Î¼g) was isolated from WT and Blimp1 CKO BMDM untreated or infected for 2 hours with L.monocytogenes (MOI=5). Three biological replicates were performed for each experimental condition. The gene chip mouse genome 430 2.0 Array (Affymetrix) was used. Biological replicates were normalized using the GCRMA method and analyzed using various Bioconductor tools.

2013-12-10 | E-GEOD-53145 | biostudies-arrayexpress

The transcriptional repressor BLIMP1 curbs host-defenses by suppressing expression of the chemokine CCL8

Project description:The transcriptional repressor BLIMP1 is a master regulator of B and T cell differentiation. To examine the role of BLIMP1 in innate immunity we used a conditional knockout (CKO) of Blimp1 in myeloid cells and found that Blimp1 CKO mice were protected from lethal infection induced by Listeria monocytogenes. Transcriptome analysis of Blimp1 CKO macrophages identified the murine chemokine (C-C motif) ligand 8, CCL8 as a direct target of Blimp1-mediated transcriptional repression in these cells. BLIMP1-deficient macrophages expressed elevated levels of Ccl8 and consequently Blimp1 CKO mice had higher levels of circulating CCL8 resulting in increased neutrophils in the peripheral blood, promoting a more aggressive anti-bacterial response. Mice lacking the Ccl8 gene were more susceptible to L. monocytogenes infection than wild type mice. While CCL8 failed to recruit neutrophils directly, it was chemotactic for γ/δ T cells and CCL8-responsive γ/δ T cells were enriched for IL-17F. Finally, CCL8-mediated enhanced clearance of L. monocytogenes was dependent on γ/δ T cells. Collectively, these data reveal an important role for BLIMP1 in modulating host-defenses by suppressing expression of the chemokine CCL8.

2013-12-10 | GSE53145 | GEO

Mapping the CCL8:P672 interface using HDX-MS

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Analysis of endothelial cells related gene in MC38 tumors

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E-GEOD-92611

Project description:Induced one gene overexpression and check the transcriptional expression

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E-GEOD-38341

Project description:Transcriptional profiling of lung cancer cells over-expression miR-34a.

2015-09-28 | E-GEOD-38341 | ExpressionAtlas

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Exploration and clinical validation of molecular typing of early colorectal cancer

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Type I interferon limits ILC2 effector functions through suppression of the CCR8-CCL1/CCL8 axis

Project description:Group 2 innate lymphoid cells (ILC2s) exert critical roles in anti-helminth immunity and the pathogenesis of allergic diseases by rapidly secreting vast amounts of type 2 signature cytokines. Type 1 interferons (IFN-I) are critical negative regulators of ILC2 effector functions and associated innate and adaptive type 2 immunopathologies. Exposure to IFN-I inhibits ILC2 proliferation as well as type 2 cytokine production, however, the mechanistic underpinnings of IFN-I-mediated ILC2 regulation remain largely elusive. Using RNA-sequencing analysis, we demonstrate that IFN-I treatment inhibits the production of the chemokine CCL1 by ILC2s. Moreover, expression of CCR8, the cognate chemokine receptor for CCL1, is downregulated upon IFN-I-stimulation ex vivo as well as in vivo upon sublethal influenza A virus infection (IAV) or upon IFN-I administration following pulmonary IL-33 challenge. In addition, expression of CCL8, the chemotactic ligand of CCR8, was suppressed in an IFN-I dependent manner in the lungs of IAV-infected mice. IFN-b potently restrained pulmonary CCL1/CCL8 expression as well as CCR8 expression by ILC2 and CD4+ T cells in a model of IL-33-driven allergic airway inflammation. Thus, this study sheds new light on the underlying mechanisms of ILC2 regulation by identifying the CCR8-CCL1/CCL8 axis as a target for IFN-I-driven ILC2 inhibition.

2025-01-15 | GSE180075 | GEO

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