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Intratumoral CpG-B promotes anti-tumoral neutrophil, cDC, and T cell cooperation without reprograming tolerogenic pDC

ABSTRACT: Intratumoral CpG-B promotes anti-tumoral neutrophil, cDC, and T cell cooperation without reprograming tolerogenic pDC

PROVIDER: PRJNA445268 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6879400.fastq.gz	Fastqsanger.gz
	SRR6879391.fastq.gz	Fastqsanger.gz
	SRR6879401.fastq.gz	Fastqsanger.gz
	SRR6879392.fastq.gz	Fastqsanger.gz
	SRR6879402.fastq.gz	Fastqsanger.gz

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Intratumoral CpG-B promotes anti-tumoral neutrophil, cDC, and T cell cooperation without reprograming tolerogenic pDC

Project description:Cancer immunotherapies utilize distinct mechanisms to harness the power of the immune system to eradicate cancer cells. Therapeutic vaccines, aimed at inducing active immune responses against an existing cancer, are highly dependent on the immunological microenvironment, where many immune cell types display high levels of plasticity and, depending on the context, promote very different immunological outcomes. Among them, plasmacytoid dendritic cells (pDC), known to be highly immunogenic upon inflammation, are maintained in a tolerogenic state by the tumor microenvironment. Here we report that intratumoral (i.t.) injection of established solid tumors with CpG oligonucleotides-B (CpG-B) inhibits tumor growth. Interestingly, control of tumor growth was independent of tumor-associated (TA) pDC, which remained refractory to CpG-B stimulation and whose depletion did not alter the efficacy of the treatment. Instead, tumor growth inhibition subsequent to i.t. CpG-B injection depended on the recruitment of neutrophils into the milieu, resulting in the activation of conventional dendritic cells (cDC), subsequent increased anti-tumor T cell priming in draining lymph nodes, and enhanced effector T cell infiltration in the tumor microenvironment. These results reinforce the concept that intratumoral delivery of TLR9 agonists alters the tumor microenvironment by improving the anti-tumor activity of both innate and adaptive immune cells.

2018-03-23 | GSE112206 | GEO

Transcriptional repression of IRF7 by MYC is critical for antiviral immune response in human pDC [pDC]

Project description:Type I interferons (IFN) are crucial mediators of human innate and adaptive immunity and are massively produced from plasmacytoid dendritic cells (pDC). IRF7 is a critical regulator of type I IFN production when pathogens are detected by TLR7/9 in pDC. However, hyperactivation of pDC can cause life-threatening autoimmune diseases. To avoid the deleterious effects of aberrant pDC activation, tight regulation of IRF7 is required. Nonetheless, the detailed mechanisms of how IRF7 transcription is regulated in pDC are still elusive. To this end, we identified the global gene expression changes after stimulation of human primary pDC with the TLR9 agonist CpGB. We identified that the transcription factor MYC is prominently upregulated upon CpGB engagement in pDC. Moreover, when we knocked down MYC in the pDC-like cell line GEN2.2, production of interferon-stimulated genes (ISGs) was dramatically increased and was further enhanced by CpGB. Interestingly, MYC is shown to be recruited to the IRF7 promoter region through interaction with NCOR2/HDAC3 for its repression, and HDAC3 inhibition enhanced IRF7 expression and IFNβ production. Interestingly, activation of TLR9-mediated NF-kB and MAPK and nuclear translocation of IRF7 were greatly enhanced by MYC depletion. Pharmaceutical inhibition of MYC recovered IRF7 expression, further confirming the negative role of MYC in the antiviral response by pDC. Furthermore, the inverse correlation of MYC and IRF7 was validated in psoriasis skin sample datasets. Therefore, our results identify the novel immunomodulatory role of MYC in human pDC and may add to our understanding of aberrant pDC function in autoimmune diseases.

2018-06-01 | GSE70277 | GEO

Gene expression in tolerogenic TGFb-treated macrophages

Project description:F4/80+ macrophages treated with TGFb2 are potently tolerogenic. Our understanding of the molecular mechanisms mediating the development of these tolerogenic properties is incomplete. We used microarray analysis to identify molecules that are involved in the tolerogenic mechanisms in murine TGFb-treated macrophages. Thioglycolate-elicited peritoneal exudate cells (F4/80+ macrophages) were treated with either PBS or TGFb2 overnight then total RNA extracted and subjected to microarray analysis.

2013-03-22 | E-GEOD-45382 | biostudies-arrayexpress

Transcription profiling of mouse immature pDC and pDC activated with CpG 1826 and influenza virus PR8

Project description:CpG 1826 binds to Toll-like receptor (TLR)9, whereas influenza virus PR8 activates pDC via TLR7. Differential stimulation of pDCs is expected to result in unique activation mechanism(s) leading to a different phenotypically and functionally matured pDC; We used microarrays to detail the global programme of gene expression underlying the maturation process of pDC activated with CpG 1826 and influenza virus PR8. We identified a distinct expression profile of upregulated immunomediators. Experiment Overall Design: Sorted pDCs were cultured for 1h and 4hs in medium control or with 5 Âµg/ml CpG 1826 or 300 HAU/ml purified influenza A/PR/8 virus. The first experiment (e1) included pDC in media and stimulated with CpG for 4h. In two other independent experimental batches (e2 and e3), we obtained samples of sorted pDC cultured in medium alone (med), and with CpG or PR8 (flu) for 1h and 4h. RNA extraction was performed using the RNeasy Kit (Qiagen) and hybridization on Affymetrix microarrays was performed using standard protocols. We sought to obtain homogeneous populations of pDCs at different time points under defined activation conditions in order to decipher the temporal resolution of expression profiles during the process of their maturation.

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Gene expression in tolerogenic TGFb-treated macrophages

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microRNA changes during Dex-induced pDC apoptosis

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Reprograming responsiveness of tolerogenic CD8+ T cells using a CXCR4 antagonist-armed oncolytic virus requires reversal of M2 macrophage polarization

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Expression data from immature pDC and pDC activated with CpG 1826 and influenza virus PR8

2007-12-13 | GSE7831 | GEO

Gene expression data from murine mDC and pDC

Project description:mDC and pDC exhibit distinct TLR expression pattern and differ in their responses to various TLR ligands. The goal of this study was to identify genes, that were differentally expressed between mDC and pDC as a means to determine how TLR signaling pathways operate. Suprisingly, expression of TLR-assoociated signaling proteins were found to be present at equivalent levels between mDC and pDC, despite differential expression of TLRs, and thus revealing insight into use of adaptor proteins that function as general regulators of TLR signaling pathways in both cell types. mDC and pDC were sorted from spleens of mice in 2 independent experiments: The first experiment included 2 replicates of pDC that were cultured in medium for 1h prior to RNA extraction and 1 replicate of mDC that were directly processed for RNA extraction after the sort. In a second experiment we obtained 2 more replicates of mDC that were processed for RNA extraction directly after the sort and run on a seperate microarray for gene expression analysis.

2014-01-01 | E-GEOD-50436 | biostudies-arrayexpress

ATAC-Seq of pDC Transcriptomes

Project description:ATAC-Seq of pDC Transcriptomes

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