Expression data for WDFY4 het vs KO cDC1 from tumor bearing mice
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE118652 | GEO | 2018/08/17
REPOSITORIES: GEO
Similar Datasets
Project description:Expression data for WDFY4 het vs KO cDC1 from tumor bearing mice
| PRJNA486346 | ENA
Project description:RNA-seq of the immune-suppressed cDC1 was done to look into the mechanism underlying TLR9. It was then compared with the inflammatory cDC1 DCs.
2021-09-03 | E-MTAB-9495 | biostudies-arrayexpress
Project description:To identify the direct targets of Zeb1 we performed ChIP-seq of wild type cDC1 cell line in unstimulated condition. cDC1 cell line was used for Chromatin Immunoprecipitation, it was then fixed and crosslinked and then fragmented and the fragmented DNA-protein was immunoprecipated using Zeb1 antibody. The chromatin sample was then used to prepare library using NEB kit following the manufacturer's protocol
2018-11-13 | E-MTAB-6917 | biostudies-arrayexpress
Project description:CD4 T cells are thought to help promote anti-tumour responses by ‘licensing’ antigen presenting cells (APCs) that activate CD8 T cells. Conventional type 1 dendritic cells (cDC1s) are responsible for cross-presentation of tumour-derived antigens to CD8 T cells. Prevailing models presume that the cDC1 is licensed by CD4 T cells that are themselves activated by a distinct cDC subset, the cDC2. The recent finding that neoantigens presented by major histocompatibility complex (MHC) class II molecules can promote rejection of tumours that lack MHC class II (MHC-II) surface expression is consistent with an indirect action of CD4 T cells, such as cDC1 licensing. However, no study has directly identified the APC that primes the CD4 T cells responsible for licensing or clearly identified the target of CD4 licensing in vivo. Here, we generated cDC1-specific Cre expressing mouse strain to inactivate or induce expression of MHC-I, MHC-II, or CD40 specifically within the cDC1 lineage. Using a tumour model that relies on CD8 T cells and CD4 T cells for rejection, we discovered that early priming of CD4 T cells against tumour-derived antigens, in contrast to soluble antigens, relied overwhelmingly on the cDC1 and not the cDC2. cDC1 do not simply transport antigen to lymph nodes for processing by cDC2, since lack of MHC-II expression on cDC1 prevented CD4 T cell priming. We also found that CD40 signaling not only affects licensing of cDC1 for CD8 T cell priming, but is also critical for the activation of CD4 T cells. Thus, in the setting of tumour-derived antigens, cDC1 can function as an autonomous platform, capable of priming both CD4 and CD8 T cells and orchestrating their cross-talk required for optimal anti-tumour immunity.
2020-06-11 | GSE152196 | GEO
Project description:Immune evasion is an important hallmark of cancer ensured by diverse strategies, including immunosuppression and downregulation of antigen presentation. Here, to restore immunogenicity of cancer cells, we employed the minimal gene regulatory network of highly immunogenic type 1 conventional dendritic cells (cDC1) to reprogram cancer cells into professional antigen presenting cells (APCs). We showed that enforced expression of PU.1, IRF8 and BATF3 (PIB) was sufficient to induce cDC1 phenotype in 33 cell lines derived from human and mouse hematological and solid tumors. PIB gradually modified the cancer cell transcriptional and epigenetic program imposing global antigen presentation and cDC1 gene signatures within 9 days. cDC1 reprogramming restored the expression of antigen presentation complexes as well as co-stimulatory molecules at the cell surface, leading to the presentation of endogenous antigens on MHC-I, and to CD8+ T cell mediated killing. Functionally, tumor- APCs acquired the ability to uptake and process exogenous proteins and dead cells, secreted inflammatory cytokines and cross-presented antigens to naïve CD8+ T cells. Importantly, tumor-APCs were efficiently generated at the single cell level from primary cancer cells of 7 solid tumors that presented antigens to memory and naïve T-cells, as well as to activated patient-specific intra-tumoral lymphocytes. Alongside antigen presentation, tumor-APCs harboring TP53, KRAS and PTEN mutations showed impaired tumorigenicity in vitro and in vivo. Finally, using in vivo mouse models of melanoma, we showed that intra-tumoral injection of tumor-APCs promoted lymphoid infiltration, delayed tumor growth and increased survival. The anti-tumor immunity elicited by tumor-APCs was synergistic with immune checkpoint inhibitors enabling tumor eradication. Our approach combines cDC1’s antigen processing and presenting abilities with endogenous generation of tumor antigens and serves as a platform for the development of novel immunotherapies based on endowed antigen presentation in cancer cells.
2023-10-24 | PXD039789 | Pride
Project description:To have a mechanistic insight how the Zeb1 KD CD8+cDC1 perturbs the immune response globally. to identify the genes that are regulated by Zeb1 RNA was isolated and check for quality, then we used NEB RNA library preparation kit to prepare the library and send for sequencing on Illumina Hi-seq 2500 platform
2018-11-13 | E-MTAB-6916 | biostudies-arrayexpress
Project description:RNA sequencing was used to characterize PGE2-mediated changes in the gene expression profile of human conventional type 1 dendritic cells (cDC1) purified from PBMCs of healthy donors. Our analysis shows that treatment of cDC1 with PGE2 induces transcriptional changes in resting cDC1. cDC1 activated with a TLR3 ligand after PGE2 pre-treatment show alterations in the expression of activation induced genes.
2023-05-27 | GSE213691 | GEO
Project description:Dendritic cells (DCs) are major regulators of innate and adaptive immune responses. DCs can be classified into plasmacytoid DCs and conventional DCs (cDCs) type 1 and 2. Murine and human cDC1 share the mRNA expression of XCR1. Murine studies indicated a specific role of the XCR1-XCL1 axis in the induction of immune responses. Here, we describe that human cDC1 can be distinguished into XCR1- and XCR1+ cDC1 in lymphoid as well as non-lymphoid tissues. Steady state XCR1+ cDC1 display a pre-activated phenotype compared to XCR1- cDC1. Upon stimulation, XCR1+ cDC1, but not XCR1- cDC1, secreted high levels of inflammatory cytokines as well as chemokines. This was associated with enhanced activation of NK cells mediated by XCR1+ cDC1. Moreover, XCR1+ cDC1 excelled in inhibiting replication of Influenza A virus. Further, under DC differentiation conditions, XCR1- cDC1 developed into XCR1+ cDC1. After acquisition of XCR1 expression, XCR1- cDC1 secreted comparable level of inflammatory cytokines. Thus, XCR1 is a marker of terminally differentiated cDC1 that licenses the antiviral effector functions of human cDC1, while XCR1- cDC1 seem to represent a late immediate precursor of cDC1.
2023-07-31 | GSE237715 | GEO
Project description:RNA sequencing was used to characterize in situ tumor infiltrating conventional type 1 dendritic cells (cDC1) in BRAFV600E melanoma tumors transplanted into C57BL/6 wildtype mice. Our analysis shows PGE2-dependent differences in the gene expression profile of intratumoral cDC1.
2023-05-27 | GSE222782 | GEO
Project description:RNA sequencing was used to characterize PGE2-mediated changes in the gene expression profile of conventional type 1 dendritic cells (cDC1). Our analysis shows that treatment of cDC1 with PGE2 or conditioned medium from PGE2-producing tumors induces transcriptional changes in resting cDC1. cDC1 activated with a TLR3 ligand after PGE2 pre-treatment show alterations in the expression of activation induced genes.
2023-05-27 | GSE213205 | GEO