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Bruton’s tyrosine kinase (BTK) and indoleamine 2,3-dioxygenase (IDO) block differentiation of inflammatory dendritic cells in tumors [Bulk RNA-seq]

ABSTRACT: Bruton’s tyrosine kinase (BTK) and indoleamine 2,3-dioxygenase (IDO) block differentiation of inflammatory dendritic cells in tumors [Bulk RNA-seq]

PROVIDER: PRJNA746314 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15123722.fastq.gz	Fastqsanger.gz
	SRR15123723.fastq.gz	Fastqsanger.gz
	SRR15123724.fastq.gz	Fastqsanger.gz

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Bruton’s tyrosine kinase (BTK) and indoleamine 2,3-dioxygenase (IDO) block differentiation of inflammatory dendritic cells in tumors [scRNA-seq]

Project description:Dendritic cells (DCs) are pivotal drivers of anti-tumor immunity, but many of the DCs in tumors appear dysfunctional or immunosuppressive. Using mouse models, we found that robustly immunogenic DCs can arise by differentiation from immature myeloid precursor cells during inflammation. In tumors, however, differentiation of these inflammatory DCs was blocked by a cell-intrinsic signaling pathway created by Bruton’s Tyrosine Kinase (BTK) and the tryptophan-degrading enzyme indoleamine 2,3-dioxygenase (IDO).

2021-08-25 | GSE180038 | GEO

Bruton’s tyrosine kinase (BTK) and indoleamine 2,3-dioxygenase (IDO) block differentiation of inflammatory dendritic cells in tumors [ATAC-seq]

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Bruton’s tyrosine kinase (BTK) and indoleamine 2,3-dioxygenase (IDO) block differentiation of inflammatory dendritic cells in tumors [Bulk RNA-seq]

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Bruton’s tyrosine kinase (BTK) and indoleamine 2,3-dioxygenase (IDO) block differentiation of inflammatory dendritic cells in tumors

Project description:Bruton’s tyrosine kinase (BTK) and indoleamine 2,3-dioxygenase (IDO) block differentiation of inflammatory dendritic cells in tumors

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Bruton’s tyrosine kinase (BTK) and indoleamine 2,3-dioxygenase (IDO) block differentiation of inflammatory dendritic cells in tumors [ATAC-seq]

Project description:Bruton’s tyrosine kinase (BTK) and indoleamine 2,3-dioxygenase (IDO) block differentiation of inflammatory dendritic cells in tumors [ATAC-seq]

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Bruton’s tyrosine kinase (BTK) and indoleamine 2,3-dioxygenase (IDO) block differentiation of inflammatory dendritic cells in tumors [scRNA-seq]

Project description:Bruton’s tyrosine kinase (BTK) and indoleamine 2,3-dioxygenase (IDO) block differentiation of inflammatory dendritic cells in tumors [scRNA-seq]

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Indoleamine 2,3-dioxygenase cannot inhibit Chlamydia trachomatis growth in HL-60 human neutrophil granulocytes

Project description:Neutrophil granulocytes are the major cells involved in the Chlamydia trachomatis (C.trachomatis)-mediated inflammation and histopathology. A key gene in human intracellular antichlamydial defense is the tryptophan degrading enzyme indoleamine 2,3-dioxygenase (IDO), which limits the growth of the tryptophan auxotroph Chlamydia. Despite its importance, the role of IDO in the intracellular defense against Chlamydia in neutrophils has not yet been characterized. Affymetrix microarrays were used to obtain global gene expression data for monitoring the effect of C. trachomatis serovar D infection on the transcriptome of human neutrophil granulocytes.

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Inhibition of Chlamydia pneumoniae Replication in Human Dendritic cells by TNF-alpha-Induced Indoleamine 2,3-Dioxygenase

Project description:Infection with Chlamydia pneumoniae, a human respiratory pathogen, has been associated with various chronic diseases such as asthma, coronary heart disease and importantly atherosclerosis. Possibly because the pathogen can exist in a persistent form. TNF-a has been reported to induce chlamydial persitence in epithelial cell lines, however the mechanism of TNF-a-induced persistence has not been reported. Moreover, C. pneumoniae persistently infect human dendritic cells (DCs) and activate DCs to produce cytokines including TNF-a. Induction of chlamydial persistence by other cytokines such as IFN-g is known to be due to indoleamine 2,3-dioxygenase (IDO) activity. The present study therefore, investigated whether C. pneumoniae infection can induce IDO activity in dendritic cells, and whether the restriction of chlamydial growth in the DCs by TNF-a is IDO-dependent. Our data indicate that infection of DCs with C. pneumoniae resulted in the induction of IDO expression. Reporting on our use of anti-TNF-a antibody adalimumab and varying concentrations of TNF-a, we further demonstrate that IDO induction following infection of DCs with C. pneumoniae is TNF-a-dependent. The anti-chlamydial activity induced by TNF-a and the expression of chlamydial 16S rRNA gene, euo, groEL1, ftsk and tal genes was correlated with the induction of IDO. Addition of excess amounts of tryptophan to the DC cultures resulted in abrogation of the TNF-a-mediated chlamydial growth restriction. These findings suggest that infection of DCs by C. pneumoniae induces production of functional IDO, which subsequently causes depletion of tryptophan. This may represent a potential mechanism for DCs to restrict bacterial growth in chlamydial infections. Keywords: Chlamydia pneumoniae, Dendritic cells, TNF-a, Indoleamine 2,3-dioxygenase

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HeLa transcriptome induction by IFN gamma and indoleamine 2,3-dioxygenase (IDO)

Project description:We describe the modulation of gene expression by IDO induction in HeLa cells.

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Bruton’s tyrosine kinase (BTK) and indoleamine 2,3-dioxygenase (IDO) block differentiation of inflammatory dendritic cells in tumors

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-08-25 | GSE180039 | GEO