Expression data from Zbtb46- CDPs, Zbtb46+ CDPs, and pre-CD8 DCs
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA509678 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Expression data from Zeb2hi CDPs, Zeb2low CDPs, and pre-CD8 DCs
| PRJNA509885 | ENA
Project description:Zbtb46 represses G-CSFR and LifR in cDCs Zbtb46 does not significantly affect gene expression in erythroid progenitors WT, Het, and KO cells were sorted from BM or spleen and analyzed. Pre MegE cells were sorted as CD117+ CD150+ CD105-CD41-CD16/32-. Pre CFU-E cells were sorted as CD117+ CD150+ CD105lo CD41- CD16/32-. CFU-E cells were sorted as CD117+ CD150- CD105+ Cd41- CD16/32-. Splenic CD4+ DCs were sorted as B220- CD11c+ MHCII+ CD8- CD172+ CD11b+ CD4+.
2012-05-20 | E-GEOD-37028 | biostudies-arrayexpress
Project description:The transcription factors Batf3 and IRF8 are required for development of CD8α+ conventional dendritic cells (cDCs), but the basis for their actions was unclear. Here, we identify two novel Zbtb46+ progenitors that separately generate CD8α+ and CD4+ cDCs and arise directly from the common DC progenitor (CDP). Irf8 expression in the CDP depends on prior PU.1-dependent autoactivation, and specification of pre-CD8 DC progenitors requires IRF8 but not Batf3. However, upon pre-CD8 DC specification, Irf8 autoactivation becomes Batf3-dependent at a CD8α+ cDC-specific enhancer containing multiple AP1-IRF composite elements (AICEs) within the Irf8 superenhancer. CDPs from Batf3-/- mice that specify toward pre-CD8 DCs fail to complete CD8α+ cDC development due to decay of Irf8 autoactivation, and divert to the CD4+ cDC lineage. Examination of histone modifications (H3K27ac and H3K4me1) and 2 transcription factors (Batf3 and Irf8) and the p300 co-factor binding in 3 different dendritic cell subsets
2015-06-08 | E-GEOD-66899 | biostudies-arrayexpress
Project description:We used microarrays to detail the programme of gene expression underlying CDP commitment to cDC1 lineage and identify differentially regulated genes during this process.
2019-06-23 | GSE123747 | GEO
Project description:Expression data from Id2-GFP- CDPs, Id2-GFP+ CDPs, Id2-GFP- pre-CD8, and Id2-GFP+ pre-CD8.
| PRJNA509888 | ENA
Project description:The transcription factors Batf3 and IRF8 are required for development of CD8α+ conventional dendritic cells (cDCs), but the basis for their actions was unclear. Here, we identify two novel Zbtb46+ progenitors that separately generate CD8α+ and CD4+ cDCs and arise directly from the common DC progenitor (CDP). Irf8 expression in the CDP depends on prior PU.1-dependent autoactivation, and specification of pre-CD8 DC progenitors requires IRF8 but not Batf3. However, upon pre-CD8 DC specification, Irf8 autoactivation becomes Batf3-dependent at a CD8α+ cDC-specific enhancer containing multiple AP1-IRF composite elements (AICEs) within the Irf8 superenhancer. CDPs from Batf3-/- mice that specify toward pre-CD8 DCs fail to complete CD8α+ cDC development due to decay of Irf8 autoactivation, and divert to the CD4+ cDC lineage.
2015-06-08 | GSE66899 | GEO
Project description:Tumor-angiogenesis and -immunity play critical roles in cancer progression and outcome. The existence of an inverse correlation hints at common regulatory mechanism(s) controlling these two processes. Here, we report that Zbtb46, a repressive transcription factor and widely accepted marker for classical dendritic cells (DCs), constitutes one such regulatory mechanism in the tumor microenvironment (TME) and is downregulated in both DCs and endothelial cells (ECs) by tumor-derived factors to facilitate robust tumor growth. This downregulation leads to the development of hallmark features of a pro-tumor environment, including dysfunctional vasculature and immunosuppressive cell accumulation. Analysis of cancer patient data revealed a similar association of a low ZBTB46 expression with an immunosuppressive TME and a worse prognosis. In contrast, upon enforced Zbtb46 expression, the hallmark TME features are mitigated, and tumor growth is restricted. Mechanistically, Zbtb46-deficient ECs were highly angiogenic, and Zbtb46-deficient bone-marrow precursors upregulated Cebpb and showed enhanced myeloid lineage output. Conversely, Zbtb46-maintenance normalizes ECs and, by suppressing Cebpb, skews the polarization of bone-marrow precursors towards more DCs and fewer macrophages, leading to an immune-hot TME. Remarkably, Zbtb46 mRNA treatment synergized with anti-PD1 immunotherapy to improve tumor management in pre-clinical models. These findings identify Zbtb46 as a common regulatory mechanism for angiogenesis and for non-hematopoietic-stem-cell-mediated myeloid lineage skewing in cancer and suggest that maintaining its expression could have therapeutic benefits.
2024-02-24 | GSE226087 | GEO
Project description:Identification of the zbtb46 interacting proteins in zebrafish DCs
2021-08-31 | PXD028191 |
Project description:Analysis of gene expressions in mouse splenic dendritic cells (DCs). DCs were purified into two subsets, CD8-positive and -negative ones. DCs were expanded in vivo by injecting Flt3L-producing tumors into the backs of C57BL/6 mice. To expand DCs in vivo, Flt3L-producing B16 melanoma cells were injected to the backs of mice. Then, 10-12 days later, splenic DCs were enriched by MACS and purified into CD3-B220-CD8a+CD11c+ and CD3-B220-CD8a-CD11c+ cells by FACS cell sorter.
2009-02-01 | E-GEOD-13250 | biostudies-arrayexpress
Project description:Cross-presentation of cell-associated antigens is carried out by classical DCs (cDCs) and monocyte-derived DCs (Mo-DCs), but whether a similar or distinct program exists for this process is unknown. In examining this issue, we discovered that only Ly-6ChiTremL4– monocytes, but not Ly-6ChiTremL4+ monocytes, can differentiate into Zbtb46+ Mo-DCs in response to GM-CSF and IL-4. However, Ly-6ChiTremL4+ monocytes were committed to Nur77-dependent development of Ly-6CloTremL4+ monocytes. Further, differentiation of monocytes with GM-CSF required addition of IL-4 to generate Zbtb46+ Mo-DCs that cross-presented as efficiently as CD24+ cDCs, which was accompanied by increased Batf3 and Irf4 expression. Unlike cDCs, Mo-DCs required only IRF4, and not Batf3, for cross-presentation. Further, Irf4–/– monocytes failed to develop into Zbtb46+ Mo-DCs, and instead developed into macrophages. Thus, cDCs and Mo-DCs use distinct transcriptional programs for cross-presentation that may drive different antigen-processing pathways. These differences may influence development of therapeutic DC vaccines based on Mo-DCs.
2016-05-25 | GSE75012 | GEO