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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE180039 | GEO | 2021/08/25

REPOSITORIES: GEO

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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]

2021-08-25 | GSE180026 | GEO

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

2021-08-25 | GSE180033 | GEO

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

| PRJNA746323 | ENA

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]

| PRJNA746405 | ENA

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]

| PRJNA746298 | ENA

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

Project description: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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Indoleamine 2,3-dioxygenase (IDO) induced by Leishmania infection of human dendritic cells.

Project description:Dendritic cells (DC) play a pivotal role in regulating immunity, establishing immunologically privileged tissue microenvironments and maintaining homoeostasis. It is becoming increasingly clear that one key mechanism that mediates many DC functions is production of the immunomodulatory enzyme indoleamine 2,3-dioxygenase (IDO). For pathogens that cause chronic infection, exploitation of host DCs is a solution to establish and persist within a host. Leishmania parasites cause a range of clinical manifestations, all involving chronic infection, and are proficient at avoiding immune responses. We demonstrate here that infection of human myeloid-derived DC with L. major and L. donovani induces IDO expression using a mechanism that involves autocrine or paracrine stimulation with a DC-secreted factor. Leishmania-induced IDO suppresses allogeneic and tetanus toxoid-specific lymphocyte proliferation, an inhibition that is reversed with the IDO inhibitor, 1-methyl tryptophan (1-MT). Furthermore, IDO expression by human DC does not require live Leishmania infection, as parasite lysates also up-regulate IDO mRNA production. Our data suggest that one mechanism Leishmania parasites utilize to circumvent immune clearance may be to promote the induction of IDO among host DC within the infection microenvironment.

| S-EPMC3572781 | biostudies-literature

A two-step induction of indoleamine 2,3 dioxygenase (IDO) activity during dendritic-cell maturation.

Project description:Prostaglandins, a family of lipidic molecules released during inflammation, display immunomodulatory properties in several models. One use includes exposure of monocyte-derived dendritic cells (DCs) to a cocktail of cytokines that contains prostaglandin E2 (PGE2) for purposes of maturation; such cells are currently being used for cancer immunotherapy trials. Our analysis of the transcription profile of DCs matured in the presence of tumor necrosis factor alpha (TNFalpha) and PGE2 revealed a strong up-regulation of indoleamine 2-3 dioxygenase (IDO), an enzyme involved in tryptophan catabolism and implicated in both maternal and T-cell tolerance. Using quantitative assays to monitor levels of IDO mRNA, protein expression, and enzyme activity, we report that PGE2 induces mRNA expression of IDO; however, a second signal through TNF receptor (TNF-R) or a Toll-like receptor (TLR) is necessary to activate the enzyme. Interestingly, use of TNFalpha, lipopolysaccharide, or Staphylococcus aureus Cowan I strain (SAC) alone does not induce IDO. The effect of PGE2 is mediated by activation of adenylate cyclase via the Gs-protein-coupled receptor E prostanoid-2 (EP2). A better understanding of these regulatory mechanisms and the crosstalk between TNF-R/TLR and EP2 signaling pathways will provide insight into the regulation of T-cell activation by DCs and may help to improve existing immunotherapy protocols.

| S-EPMC1895261 | biostudies-literature

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.

2017-02-09 | GSE75956 | GEO