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IRF8-regulated genes in primary CD11 b cells

ABSTRACT: Transcriptional profiling of IRF8-regulated genes in mouse CD11b-positive primary cells. CD11b-positive cells were isolated from spleens of age-matched wt and IRF8 KO mice, the compared for their gene expression profiles. The objective is to identify genes that are regulated by IRF8 in CD11b-positive primary cells. Two-condition experiments. Wt vs IRF8 KO cells. Biological replicates: 2 replicates for the comparison.

ORGANISM(S): Mus musculus

SUBMITTER: Kebin Liu

PROVIDER: E-GEOD-31464 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Cutting edge: IRF8 regulates Bax transcription in vivo in primary myeloid cells.

Yang Jine J Hu Xiaolin X Zimmerman Mary M Torres Christina M CM Yang Dafeng D Smith Sylvia B SB Liu Kebin K

Journal of immunology (Baltimore, Md. : 1950) 20110926 9

A prominent phenotype of IRF8 knockout (KO) mice is the uncontrolled expansion of immature myeloid cells. The molecular mechanism underlying this myeloproliferative syndrome is still elusive. In this study, we observed that Bax expression level is low in bone marrow preginitor cells and increases dramatically in primary myeloid cells in wt mice. In contrast, Bax expression level remained at a low level in primarymyeloid cells in IRF8 KO mice. However, in vitro IRF8 KO bone marrow-differentiated ...[more]

PMID: 21949018

Similar Datasets

IRF8-regulated genes in primary CD11 b cells

Project description:Transcriptional profiling of IRF8-regulated genes in mouse CD11b-positive primary cells. CD11b-positive cells were isolated from spleens of age-matched wt and IRF8 KO mice, the compared for their gene expression profiles. The objective is to identify genes that are regulated by IRF8 in CD11b-positive primary cells.

2011-10-20 | GSE31464 | GEO

CoCl2 Response in Cryptococcus neoformans

Project description:We investigated the effects of the hypoxia-mimetic CoCl2 on the gene expression of pathogenic fungus Cryptococcus neoformans. Keywords: compound treatment design Three biological repeats were performed using three independent RNA sets isolated from cells cultured on different days and the dye-reverse hybridizations were performed for all three sets. One set of RNA was also subjected to technical repeats.

2010-05-19 | E-GEOD-11390 | biostudies-arrayexpress

Role for ISGF3II in the Antiviral Activity of IFN-gamma

Project description:Type-I (e.g. IFN-alpha, IFN-beta) and type-II IFNs (IFN-gamma) have antiviral, antiproliferative, and immunomodulatory properties. Both types of IFN signal through the Jak/STAT pathway to elicit antiviral activity, yet IFN-gamma is thought to do so only through STAT1 homodimers while type-I IFNs activate both STAT1- and STAT2-containing complexes such as ISGF3. Here we show that ISGF3II - composed of phosphorylated STAT1, unphosphorylated STAT2, and IRF9 - also plays a role in IFN-gamma-mediated antiviral activity in humans. Using phosphorylated STAT1 as a marker for IFN signaling, western blot analysis of IFN-alpha2a treated human A549 cells revealed that pSTAT1 (Y701) levels peaked at 1h, decreased by 6h, and remained at low levels for up to 48h. Cells treated with IFN-gamma showed a biphasic pSTAT1 response with an early peak at 1-2h and a second peak at 15-24h. Gene expression microarray following IFN-gamma treatment for 24h indicated an induction of antiviral genes that are induced by ISGF3 and associated with a type-1 IFN response. Induction of these genes by autocrine type-I and type-III IFN signaling was ruled out using neutralizing antibodies to these IFNs in biological assays and by qRT-PCR. Despite the absence of autocrine IFNs, IFN-gamma treatment induced formation of ISGF3II. This novel transcription factor complex binds to ISRE promoter sequences, as shown by ChIP analysis of the PKR promoter. STAT2 and IRF9 knockdown in A549 cells reversed IFN-gamma-mediated ISRE induction and antiviral activity - implicating ISGF3II formation as a significant component of the cellular response and biological activity of IFN-gamma. Two treatments using three biological replicates each were performed using three million A549 cells. Each was seeded overnight in 10mL complete RPMI and treated. Three were treated with alpha-IFN and three treated with gamma-IFN for 24h. Control samples were left untreated.

2011-01-19 | E-GEOD-25113 | biostudies-arrayexpress

The Candida glabrata transcription factor Stb5p is a negative regulator of ATP-binding cassette transporters

Project description:The opportunistic yeast pathogen Candida glabrata is recognized for its ability to acquire resistance during prolonged treatment with azole antifungals. Resistance to azoles is largely mediated by the transcription factor PDR1, resulting in the upregulation of ATP-binding cassette (ABC) transporter proteins and drug efflux. Studies in the related yeast Saccharomyces cerevisiae have shown Pdr1p forms a heterodimer with another transcription factor, Stb5p. In C. glabrata the ORF designated CAGL0I02552g has 38.8% amino acid identity with STB5 (YHR178w), and shares an N-terminal Zn2Cys6 binuclear cluster domain and a fungal specific transcriptional factor domain, prompting us to test for homologous function and a possible role in azole resistance. Complementation of deltayhr178w (stb5) with CAGL0I02552g resolved the increased sensitivity to cold, hydrogen peroxide and caffeine of the mutant, for which reason we designated CAGl0I02552g as CgSTB5. Overexpression of CgSTB5 in C. glabrata repressed azole resistance, whereas deletion of CgSTB5 increased resistance, both by a mechanism independent of CgPDR1. Expression analysis found that CgSTB5 shares many of the same transcriptional targets as CgPDR1 but, unlike the later, is a negative regulator of pleiotropic drug resistance, including the ABC transporter genes CDR1,PDH1, and YOR1. The CgPDR1OE (n=5) arrays consisted of five technical repeats with one prepared using reciprocal labeling. The Cgstb5delta (n=4) and CgSTB5OE (n=4) arrays consisted of four technical repeats each with one prepared using reciprocal labeling.

2013-03-11 | E-GEOD-37071 | biostudies-arrayexpress

IRF8 regulates intrinsic ferroptosis through repressing p53 expression to maintain tumor cell sensitivity to cytotoxic T lymphocytes

Project description:Ferroptosis has emerged as a cytotoxic T lymphocyte (CTL)-induced tumor cell death pathway. The regulation of tumor cell sensitivity to ferroptosis is still incompletely understood. We report here that the interferon regulatory factor 8 (IRF8) functions as a regulator of tumor cell intrinsic ferroptosis. Genome-wide gene expression profiling identified ferroptosis pathway as an IRF8-regulated pathway in tumor cells. IRF8.KO tumor cells acquire resistance to intrinsic ferroptosis induction and IRF8-deficient tumor cells exhibit decreased ferroptosis in response to tumor-specific CTLs. Irf8 deletion increases p53 expression in tumor cells and knocking out p53 in IRF8.KO tumor cells restored tumor cell sensitivity to intrinsic ferroptosis induction. Furthermore, IRF8.KO tumor cells grew significantly faster than WT tumor cells in immune competent mice. To restore IRF8 expression in tumor cells, we designed and synthesized codon usage-optimized IRF8-encoding DNA to generate IRF8-encoding plasmid NTC9385R-mIRF8. Restoring IRF8 expression via a lipid nanoparticle-encapsulated NTC9385R-mIRF8 plasmid therapy suppressed established tumor growth in vivo. In human cancer patients, nivolumab responders have a significant higher IRF8 expression level in their tumor cells as compared to the non-responders. Our data determine that IRF8 represses p53 expression to maintain tumor cell sensitivity to intrinsic ferroptosis

2022-09-25 | GSE213856 | GEO

Profiling of filarial induced genes in lymphatic endothelial cells

Project description:To observe the global changes in the lymphatic endothelial cells upon exposure to filarial antigens or parasites, LECs were stimulated for 24, 48, and 72hrs and the expression profiles were carried out. Human filarial parasites Brugia malayi and Wuchereria bancrofti habitat the lymphatics and cause lymphatic dilatation and lymphedema. In order to evaluate the effect of various stage specific effects on the lymphatic endothelial cells (LEC) and understand how they modulate the lymphatic dysfunction, LECs were stimulated in antigens derived from the Brugia malayi. These are preliminary time course data towards understanding how the filarial antigens induce lymphangiogenesis.

2010-05-19 | E-GEOD-15454 | biostudies-arrayexpress

Gene expression profiling of spleen marginal zone B cells and spleen follicular B cells in IRF8 conditional KO mice

Project description:Conditional IRF8 KO mice (mice with a conditional allele of Irf8 crossed with CD19-Cre mice) showed increased numbers of both Gene expression data spleen marginal zone (MZ) and Gene expression data spleen follicular (FO) B cells compared to control mice. To evaluate gene expression patterns that distinguished FO or MZ B cells derived from conditional KO and control mice, we used Affymetrix GeneChip® Mouse gene 1.0 ST Array. FACS-sorted MZ and FO B cells from individual mouse were used for RNA extraction and Affyarray hybridization. There were six independent biological replications in each group - six cases of MZ B cells and FO cells in IRF8 conditional KO mice and six cases of MZ B cells and FO cells in control WT mice.

2010-12-20 | E-GEOD-24972 | biostudies-arrayexpress

A lncRNA identifies Irf8 enhancer element in negative feedback control of dendritic cell differentiation

Project description:Dendritic cells (DC) are professional antigen presenting cells that develop from multipotent progenitors (MPP) and DC committed common DC progenitors (CDP) and further differentiate into different subsets: classical DC type 1 and 2 (cDC1 and cDC2, respectively) and plasmacytoid DC (pDC). In this study MPP, CDP, cDC1, cDC2 and pDC were obtained in a two-step in vitro culture system according to Felker et al., J. Immunol. 185, 5326-5335, 2010. Briefly, mouse bone marrow cells were first amplified with a specific cytokine cocktail and then induced to differentiate into DC with Flt3 ligand. MPP, CDP, cDC1, cDC2 and pDC were obtained by FACS sorting as follows: MPP: Gr1- CD117hi CD135low/-; CDP: Gr1- CD117int CD135+ CD115+; cDC1: CD11c+ CD11blow/- XCR1+; cDC2: CD11c+ CD11b+ XCR1- and pDC: CD11c+ CD11b- B220+. FACS sorted cells were then subjected to Omni-ATAC-seq, nuclear-titrated (NuTi) Capture-C targeting Irf8 promoter, and RNA-seq analysis. ATAC-seq data of cDC1 and pDC are published (Li et al., Genome Biol. 20, 45, 2019; GSE118221). ATAC-seq data of MPP, CDP and cDC2, NuTi Capture-C and RNA-seq data of MPP, CDP, cDC1, cDC2 and pDC are published here. CD11c+ CD11b+ B220- cDC and CD11c+ CD11b- B220+ pDC were obtained by FACS sorting and subjected to ChIP-seq analysis of IRF8 and are published here.

2023-03-01 | GSE198651 | GEO

The HAT Inhibitor Anacardic Acid Leads to Changes in Global Gene Expression During in vitro P.falciparum Development

Project description:To better understand the role of histone lysine acetylation in transcription in Plasmodium falciparum, we sought to attenuate the histone acetyltransferase (HAT) activity of PfGCN5 using anacardic acid (AA). We showed that AA reversibly and noncompetitively inhibited the HAT activity of recombinant PfGCN5. To a lesser extent, AA inhibited the PfGCN5 activity in parasite nuclear extracts, but did not affect the histone deacetylase activity. AA blocked the growth of both chloroquine-sensitive and -resistant strains with a 50% inhibitory concentration of ~30 uM. Treatment of the parasites with 20 uM of AA for 12 h had no obvious effect on parasite growth or gross morphology, but induced hypoacetylation of histone H3 at K9 and K14, but not H4 at K5, K8, K12, and K16, suggesting of specific inhibition of the PfGCN5 HAT. Microarray analysis showed that this AA treatment disturbed the parasite transcription program, resulting in â¥2-fold change in the expression of 271 (~5%) parasite genes in late trophozoites, among which 207 genes were down-regulated. Interestingly, a significant proportion of the down-regulated genes is potentially associated with signal transduction and transcription. Furthermore, cluster analysis of gene expression indicated that AA mostly down-regulated active genes, and this gene pool significantly overlapped with that enriched for H3K9 acetylation. We further demonstrated by chromatin immunoprecipitation and real-time polymerase chain reaction that AA treatment reduced acetylation near the putative promoters of a set of down-regulated genes. The identification of AA as a PfGCN5 inhibitor offers a useful tool for further functional analysis of epigenetics in transcription regulation in malaria parasites. Late trophozoits were selected after AA treatment or untreated for RNA extraction and hybridization on microarrays. We sought to obtain the expression level changing after AA treatment.

2008-06-13 | E-GEOD-11763 | biostudies-arrayexpress