Mus musculus
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-53145
PROVIDER: PRJNA231003 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The transcriptional repressor BLIMP1 curbs host-defenses by suppressing expression of the chemokine CCL8
2015-07-31 | E-GEOD-53145 | ExpressionAtlas
Project description:The transcriptional repressor BLIMP1 is a master regulator of B and T cell differentiation. To examine the role of BLIMP1 in innate immunity we used a conditional knockout (CKO) of Blimp1 in myeloid cells and found that Blimp1 CKO mice were protected from lethal infection induced by Listeria monocytogenes. Transcriptome analysis of Blimp1 CKO macrophages identified the murine chemokine (C-C motif) ligand 8, CCL8 as a direct target of Blimp1-mediated transcriptional repression in these cells. BLIMP1-deficient macrophages expressed elevated levels of Ccl8 and consequently Blimp1 CKO mice had higher levels of circulating CCL8 resulting in increased neutrophils in the peripheral blood, promoting a more aggressive anti-bacterial response. Mice lacking the Ccl8 gene were more susceptible to L. monocytogenes infection than wild type mice. While CCL8 failed to recruit neutrophils directly, it was chemotactic for γ/δ T cells and CCL8-responsive γ/δ T cells were enriched for IL-17F. Finally, CCL8-mediated enhanced clearance of L. monocytogenes was dependent on γ/δ T cells. Collectively, these data reveal an important role for BLIMP1 in modulating host-defenses by suppressing expression of the chemokine CCL8. RNA (5μg) was isolated from WT and Blimp1 CKO BMDM untreated or infected for 2 hours with L.monocytogenes (MOI=5). Three biological replicates were performed for each experimental condition. The gene chip mouse genome 430 2.0 Array (Affymetrix) was used. Biological replicates were normalized using the GCRMA method and analyzed using various Bioconductor tools.
2013-12-10 | E-GEOD-53145 | biostudies-arrayexpress
Project description:The transcriptional repressor BLIMP1 is a master regulator of B and T cell differentiation. To examine the role of BLIMP1 in innate immunity we used a conditional knockout (CKO) of Blimp1 in myeloid cells and found that Blimp1 CKO mice were protected from lethal infection induced by Listeria monocytogenes. Transcriptome analysis of Blimp1 CKO macrophages identified the murine chemokine (C-C motif) ligand 8, CCL8 as a direct target of Blimp1-mediated transcriptional repression in these cells. BLIMP1-deficient macrophages expressed elevated levels of Ccl8 and consequently Blimp1 CKO mice had higher levels of circulating CCL8 resulting in increased neutrophils in the peripheral blood, promoting a more aggressive anti-bacterial response. Mice lacking the Ccl8 gene were more susceptible to L. monocytogenes infection than wild type mice. While CCL8 failed to recruit neutrophils directly, it was chemotactic for γ/δ T cells and CCL8-responsive γ/δ T cells were enriched for IL-17F. Finally, CCL8-mediated enhanced clearance of L. monocytogenes was dependent on γ/δ T cells. Collectively, these data reveal an important role for BLIMP1 in modulating host-defenses by suppressing expression of the chemokine CCL8.
2013-12-10 | GSE53145 | GEO
Project description:The transcriptional repressor Blimp1/Prdm1 regulates post-natal reprogramming of intestinal enterocytes
| PRJNA141251 | ENA
Project description:We use HDX-MS to characterise the binding interface between the tick evasin P672 and the chemokine CCL8, in order to assist in the development of peptides capable of mimicking P672 anti-inflammatory activity.
2020-05-29 | PXD019199 | Pride
Project description:To clarify the potential BLIMP1 downstream target regulating PD-L1 expression, we performed proteomics analysis using BLIMP1 Hep3B cells and control cells. Proteomics analysis revealed that SPI1 may serve as a pivotal transcriptional factor that enhances PD-L1 expression by acting as a downstream effector of BLIMP1.
2022-11-23 | PXD037621 | Pride
Project description:We show that endothelial cells from MC38 tumors in WT mice express high chemokine Ccl8 than in Apelin knockout mice. We found that Apelin induces Ccl8 expression in ECs and enhances anti-tumor immunity.
2021-06-23 | GSE178681 | GEO
Project description:Early detection of viral infection and rapid activation of host antiviral defenses are critical for limiting viral replication and spread. At a cellular level, this is achieved through host pattern recognition receptors that sense viral nucleic acid as foreign and initiate antiviral defenses through transcriptional upregulation of antiviral cytokines interferons (IFNs) and interferon stimulated genes (ISGs). However, aberrant production of IFN in the absence of viral infection leads to auto-inflammation and can be detrimental to the host. Here, we show that the DNA binding transcriptional repressor complex composed of Capicua (CIC) and Ataxin-1 like (ATXN1L) bind to 8-nucleotide motif near IFN and ISG promoters and block aberrant expression under homeostasis. However, during respiratory viral infections, this active repression is relieved by rapid degradation of the CIC-ATXN1L complex via the activation Mitogen‑activated protein kinase (MAPK) pathway, thereby priming the host cells ready to mount robust antiviral responses through canonical interferon regulatory factors (IRF), and signal transducer and activator of transcription (STAT) transcription factors. Importantly, murine Cic-Atxn1L also repress expression from IFN and ISGs promoters, demonstrating the conservation of this regulatory mechanism in murine species. Together, our studies define a new paradigm for regulation of IFN and ISGs through the evolutionarily conserved CIC-ATXN1L DNA binding transcription repressor complex under homeostasis and viral infection conditions.
2025-03-24 | GSE271899 | GEO
Project description:Early detection of viral infection and rapid activation of host antiviral defenses are critical for limiting viral replication and spread. At a cellular level, this is achieved through host pattern recognition receptors that sense viral nucleic acid as foreign and initiate antiviral defenses through transcriptional upregulation of antiviral cytokines interferons (IFNs) and interferon stimulated genes (ISGs). However, aberrant production of IFN in the absence of viral infection leads to auto-inflammation and can be detrimental to the host. Here, we show that the DNA binding transcriptional repressor complex composed of Capicua (CIC) and Ataxin-1 like (ATXN1L) bind to 8-nucleotide motif near IFN and ISG promoters and block aberrant expression under homeostasis. However, during respiratory viral infections, this active repression is relieved by rapid degradation of the CIC-ATXN1L complex via the activation Mitogen‑activated protein kinase (MAPK) pathway, thereby priming the host cells ready to mount robust antiviral responses through canonical interferon regulatory factors (IRF), and signal transducer and activator of transcription (STAT) transcription factors. Importantly, murine Cic-Atxn1L also repress expression from IFN and ISGs promoters, demonstrating the conservation of this regulatory mechanism in murine species. Together, our studies define a new paradigm for regulation of IFN and ISGs through the evolutionarily conserved CIC-ATXN1L DNA binding transcription repressor complex under homeostasis and viral infection conditions.
2025-03-24 | GSE271898 | GEO
Project description:Early detection of viral infection and rapid activation of host antiviral defenses are critical for limiting viral replication and spread. At a cellular level, this is achieved through host pattern recognition receptors that sense viral nucleic acid as foreign and initiate antiviral defenses through transcriptional upregulation of antiviral cytokines interferons (IFNs) and interferon stimulated genes (ISGs). However, aberrant production of IFN in the absence of viral infection leads to auto-inflammation and can be detrimental to the host. Here, we show that the DNA binding transcriptional repressor complex composed of Capicua (CIC) and Ataxin-1 like (ATXN1L) bind to 8-nucleotide motif near IFN and ISG promoters and block aberrant expression under homeostasis. However, during respiratory viral infections, this active repression is relieved by rapid degradation of the CIC-ATXN1L complex via the activation Mitogen‑activated protein kinase (MAPK) pathway, thereby priming the host cells ready to mount robust antiviral responses through canonical interferon regulatory factors (IRF), and signal transducer and activator of transcription (STAT) transcription factors. Importantly, murine Cic-Atxn1L also repress expression from IFN and ISGs promoters, demonstrating the conservation of this regulatory mechanism in murine species. Together, our studies define a new paradigm for regulation of IFN and ISGs through the evolutionarily conserved CIC-ATXN1L DNA binding transcription repressor complex under homeostasis and viral infection conditions.
2025-03-24 | GSE271897 | GEO