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Cancerous inhibitor of Protein Phosphatase 2A promotes B-cell activation in vitro

ABSTRACT: The generation of optimal immune response requires combined activation of both T- and B-cells. Here, we demonstrate that the cancerous inhibitor of protein phosphatase 2A (CIP2A) is a novel factor that governs activation of both T- and B-cells in vivo. Upon ovalbumin challenge, CIP2A-deficient (CIP2AHOZ) mice show impaired immune response. Furthermore, CIP2AHOZ mice had impaired clearance of Listeria Monocytogenesis (L.m.) infection, combined with decreased numbers of CD8+ T-cells and IFN-γ secretion. In an ovalbumin model of allergic asthma, CIP2AHOZ B-cells were impaired in IgE and IgG secretion, despite of normal Th2 differentiation and unaffected numbers of inflammatory cells or cytokines in bronchoalveolar lavage. Importantly, the cell-autonomous effect of CIP2A deficiency for both T- and B-cell activation was confirmed by in vitro assays. During the T-cell activation CIP2A, was shown to promote expression of ETS-1, whereas in B-cells CIP2A loss resulted in inhibition of MYC-mediated gene expression. Together these results identify CIP2A as a novel cell-autonomous regulator governing both T- and B-cell activation in vivo. They also identify CIP2AHOZ as a novel murine model for investigation of impaired immune response and allergic asthma.

ORGANISM(S): Mus musculus

PROVIDER: GSE63391 | GEO | 2015/12/01

SECONDARY ACCESSION(S): PRJNA267651

REPOSITORIES: GEO

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Cancerous inhibitor of Protein Phosphatase 2A is a novel cell-autonomous regulator governing both T-and B-cell activation in vivo

Project description:The generation of optimal immune response requires combined activation of both T- and B-cells. Here, we demonstrate that the cancerous inhibitor of protein phosphatase 2A (CIP2A) is a novel factor that governs activation of both T- and B-cells in vivo. Upon ovalbumin challenge, CIP2A-deficient (CIP2AHOZ) mice show impaired immune response. Furthermore, CIP2AHOZ mice had impaired clearance of Listeria Monocytogenesis (L.m.) infection, combined with decreased numbers of CD8+ T-cells and IFN-? secretion. In an ovalbumin model of allergic asthma, CIP2AHOZ B-cells were impaired in IgE and IgG secretion, despite of normal Th2 differentiation and unaffected numbers of inflammatory cells or cytokines in bronchoalveolar lavage. Importantly, the cell-autonomous effect of CIP2A deficiency for both T- and B-cell activation was confirmed by in vitro assays. During the T-cell activation CIP2A, was shown to promote expression of ETS-1, whereas in B-cells CIP2A loss resulted in inhibition of MYC-mediated gene expression. Together these results identify CIP2A as a novel cell-autonomous regulator governing both T- and B-cell activation in vivo. They also identify CIP2AHOZ as a novel murine model for investigation of impaired immune response and allergic asthma. Total RNA obtained from 4 male mutant mice was compared to 4 wild type controls.

2015-06-10 | E-GEOD-56401 | biostudies-arrayexpress

Cancerous inhibitor of Protein Phosphatase 2A is a novel cell-autonomous regulator governing both T-and B-cell activation in vivo

Project description:The generation of optimal immune response requires combined activation of both T- and B-cells. Here, we demonstrate that the cancerous inhibitor of protein phosphatase 2A (CIP2A) is a novel factor that governs activation of both T- and B-cells in vivo. Upon ovalbumin challenge, CIP2A-deficient (CIP2AHOZ) mice show impaired immune response. Furthermore, CIP2AHOZ mice had impaired clearance of Listeria Monocytogenesis (L.m.) infection, combined with decreased numbers of CD8+ T-cells and IFN-γ secretion. In an ovalbumin model of allergic asthma, CIP2AHOZ B-cells were impaired in IgE and IgG secretion, despite of normal Th2 differentiation and unaffected numbers of inflammatory cells or cytokines in bronchoalveolar lavage. Importantly, the cell-autonomous effect of CIP2A deficiency for both T- and B-cell activation was confirmed by in vitro assays. During the T-cell activation CIP2A, was shown to promote expression of ETS-1, whereas in B-cells CIP2A loss resulted in inhibition of MYC-mediated gene expression. Together these results identify CIP2A as a novel cell-autonomous regulator governing both T- and B-cell activation in vivo. They also identify CIP2AHOZ as a novel murine model for investigation of impaired immune response and allergic asthma.

2015-06-10 | GSE56401 | GEO

Ovalbumin sensitized and challenged induces differential gene expression in mouse lungs

Project description:To gain insight into the promoting effect of ultrafine particle inhalation on development and progression of allergic asthma, we selected an experimental approach involving exposure to ultrafine carbon particles (UCP) and gene expression profiling of lungs from mice with experimental, ovalbumin induced allergy. Comparative gene expression analysis was performed by hybridizing pooled cDNA samples from lavaged lungs of different groups. These results suggest that allergic sensitization may represent a susceptibility factor for effects of UCP on gene expression in the lung. In sensitized individuals UCP exposure, such as found in polluted air, thus may contribute to the development and /or aggravation of allergic asthma. Keywords: Particle Inhalation, lung, ovalbumin sensitzed and challanged, experssion profiling Lungs of groups of six non-sensitized, ovalbumin sensitized, or sensitized and ovalbumin challenged BALB/cJ mice, either subjected to particle-free or UCP containing air; two replicates including one dye swap experiment have been performed for lungs: a) non-sensitized particle free air versus sensitized and ovalbumin challenged sensitized particle free air; b) non-sensitized UCP containing air versus sensitized and ovalbumin challenged sensitized UCP containing air

2010-06-10 | E-GEOD-6496 | biostudies-arrayexpress

MeRIP Sequencing of Lung Tissues from OVA‐induced Acute Allergic Asthma Mice

Project description:The objective of the study was to present a transcriptome-wide m6A methylome profile of lung tissues in mouse model of ovalbumin(OVA)-induced acute allergic asthma.

2021-10-11 | GSE179874 | GEO

UCP exposure of ovalbumin sensitized and challenged mice

2007-07-01 | GSE6571 | GEO

Ovalbumin sensitized and challenged induces differential gene expression in mouse lungs

2007-07-01 | GSE6496 | GEO

De novo fatty acid synthesis in invariant NKT cells is critical for the development of airway hyperresponsiveness

Project description:Allergic responses in airway against house dust mites (HDMs) depend on lipid metabolism. However, whether the state of lipid metabolism in iNKT cells serves as a critical mechanism to impact development of allergic asthma remains elusive. Here, we showed that acetyl-CoA-Carboxylase 1 (ACC1), a key enzyme for fatty acid synthesis, was highly expressed in iNKT cells from asthmatic lungs. In ovalbumin (OVA)- and HDM-induced allergic asthma models, Cd4-CreAcc1fl/fl mice exhibited impaired homeostasis of iNKT cells and failed to develop AHR. ACC1-deficient iNKT cells reduced intracellular lipid concentration and expression of fatty acid binding proteins (FABPs) and peroxisome proliferator-activated receptor-gamma (PPAR-γ), whereas these cells were increased in glycolytic capacity. Moreover, ACC1-FABP-PPAR-γ axis regulated cell death of ACC1-deficient iNKT cells. Adoptive transfer of wild type (WT) iNKT cells restored AHR in Jɑ18 knockout mice in OVA or HDM-induced asthma models, whereas that of ACC1-deficient iNKT cells did not, indicating that fatty acid synthesis in iNKT cells is one of main contributors to the development of AHR. Our finding demonstrate fatty acid metabolism in iNKT cells is critical contributor for the development of AHR and airway inflammation in asthma.

2022-06-15 | GSE205761 | GEO

Transcriptional profiling of TH2 cells identifies pathogenic features associated with asthma

Project description:Allergic asthma and rhinitis are two common chronic allergic diseases that affect the lungs and nose, respectively. Both diseases share clinical and pathological features characteristic of excessive allergen-induced type 2 inflammation, orchestrated by memory CD4+ T cells that produce type 2 cytokines (TH2 cells). However, a large majority of subjects with allergic rhinitis do not develop asthma, suggesting divergence in disease mechanisms. Since TH2 cells play a pathogenic role in both these diseases and are also present in healthy non-allergic subjects, we performed global transcriptional profiling to determine whether there are qualitative differences in TH2 cells from subjects with allergic asthma, rhinitis and healthy controls. TH2 cells from asthmatic subjects expressed higher levels of several genes that promote their survival as well as alter their metabolic pathways to favor persistence at sites of allergic inflammation. In addition, genes that enhanced TH2 polarization and TH2 cytokine production were also upregulated in asthma. Several genes that oppose T cell activation were downregulated in asthma, suggesting enhanced activation potential of TH2 cells from asthmatic subjects. Many novel genes with poorly defined functions were also differentially expressed in asthma. Thus, our transcriptomic analysis of circulating TH2 cells has identified several molecules that are likely to confer pathogenic features to TH2 cells that are either unique or common to both asthma and rhinitis.

2016-06-01 | GSE75011 | GEO

UCP exposure of ovalbumin sensitized and challenged mice

Project description:To gain insight into the promoting effect of ultrafine particle inhalation on development and progression of allergic asthma, we selected an experimental approach involving exposure to ultrafine carbon particles (UCP) and gene expression profiling of lungs from mice with experimental, ovalbumin induced allergy. Comparative gene expression analysis was performed by hybridizing pooled cDNA samples from lavaged lungs of different groups. The results suggest that allergic sensitization may represent an susceptibility factor for effects of UCP on gene expression in the lung. In sensitized individuals UCP exposure, such as found in polluted air, thus may contribute to the development and/or aggrevation of allergic asthma. Keywords: Particle Inhalation, lung, ovalbumin sensitized and challanged, expression profling Lungs of groups of six sensitized or sensitized and challanged BALB/cJ mice, either subjected to particle-free or UCP containing air; two replicates including one dye swap experiment have been performed for lungs: a) sensitized particle free air versus sensitized UCP exposure; b) sensitized and challanged particle free air versus sensitized and challanged UCP exposure

2010-06-10 | E-GEOD-6571 | biostudies-arrayexpress

Intranasal administration of OM-85, a bacterial lysate, alters lung transcriptional profiles and protects against experimental asthma

Project description:Background: Microbial interventions against allergic asthma have robust epidemiologic underpinnings and the potential to recalibrate disease-inducing immune responses. Oral administration of OM-85, a standardized lysate of human airways bacteria, is widely used empirically to prevent respiratory infections, and a clinical trial is testing its ability to prevent asthma in at-risk children. On the other hand, we previously showed that intra-nasal administration of products from microbe-rich farm environments abrogate experimental allergic asthma. Objectives: To investigate whether direct administration of OM-85 to the airway compartment protects against experimental allergic asthma, and to identify protective cellular and molecular mechanisms activated through this natural route. Methods: BALB/cJ mice (7-8 weeks old) sensitized and challenged with Ovalbumin received OM-85 intra-nasally, and cardinal cellular and molecular asthma phenotypes were measured. Murine lung gene expression was profiled by RNA-sequencing. Results: Airway administration of OM-85 suppressed allergic asthma and altered the transcriptome profile in unfractionated lung tissue. Conclusion We provide the first demonstration that administration of a standardized bacterial lysate to the airway compartment protects from experimental allergic asthma by engaging multiple immune pathways.

2021-10-19 | GSE167867 | GEO

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