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Expression data from liver of Recombinant human IgG1 treated high-fat-diet-induced ApoE-/- mice

ABSTRACT: On the basis of the clear role of Recombinant human IgG1 in the reduction of liver triglyceride (TG) level elevated by high-fat-diet, the potential effector genes of Recombinant human IgG1 are screened by means of transcriptional techniques.

ORGANISM(S): Mus musculus

PROVIDER: GSE190421 | GEO | 2022/12/12

REPOSITORIES: GEO

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Expression data from liver of Recombinant human IgG1 treated high-fat-diet-induced ApoE-/- mice

Project description:Expression data from liver of Recombinant human IgG1 treated high-fat-diet-induced ApoE-/- mice

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Genome-wide analysis of SAK-HV treatment caused hepatic genes expression in ApoE knockout mice

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Transcriptome analysis of mouse IgG1 memory B cell subsets

Project description:IgE plays an essential role in the pathogenesis of allergies and its production is strongly regulated. A transient IgE germinal center phase and lack of IgE memory cells limit the generation of pathogenic IgE, but this can be overcome by sequential switching of IgG1 cells to IgE. We investigated which population of IgG1 cells can give rise to IgE-producing cells in memory responses. We identified three populations of IgG1 memory B cells (DP:CD73+CD80+, SP:CD73-CD80+, DN:CD73-CD80-) that generate IgE plasma cells of high or low affinity, but none gives rise to IgE germinal center cells or IgE memory cells. The two memory IgG1 populations differ however in their ability to differentiate into IgG1 plasma cells and germinal center cells, and to expand the IgG1 memory B cell pool. To explore the molecular mechanisms that may explain the distinct functions of IgG1 memory B cell subsets we compared their expression by transcriptome analysis using next generation sequencing.

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Expression data from IgE+ and IgG1+ B lymphocytes in mice infected with Nippostrongylus brasiliensis

Project description:The mechanisms involved in the maintenance of memory IgE responses are poorly understood, and the role played by germinal center (GC) IgE cells in these memory responses is particularly unclear. IgE B-cell differentiation is characterized by a transient GC phase, a bias towards the plasma cell (PC) fate, and dependence on sequential switching for the production of high-affinity IgE. We show here that IgE GC B cells are unfit to undergo the conventional GC differentiation program due to impaired B-cell receptor function and increased apoptosis. IgE GC cells fail to populate the GC light zone and are unable to contribute to the memory and long-lived PC compartments. Furthermore, we demonstrate that direct and sequential switching are linked to distinct B-cell differentiation fates: direct switching generates IgE GC cells, whereas sequential switching gives rise to IgE plasma cells. We propose a comprehensive model for the generation and memory of IgE responses. The purpose of this analysis was to: 1) identify expression differences between IgE and IgG1 B lymphocytes, 2) identify GC Dark Zone (DZ) and Light Zone (LZ) signatures of IgG1 GC cells. For that purpose, we compared in one experiment the gene expression patterns of IgE germinal center (GC) cells, IgG1 GC cells, IgE plasma cells (PC), IgG1 PC and naïve cells. In a second experiment, we compared the expression of IgG1 DZ GC cells with that of IgG1 LZ GC cells. Triplicates obtained from independent sorting experiments were used for all samples except two (IgG1 PC=2 samples; IgE PC=4 samples). Each sample was obtained from a pool of three individual mice. The mice used in the experiment were CeGFP BALB/c mice infected with the parasite N. brasiliensis. CeGFP mice carry an IRES-GFP KI cassette in the 3'UTR of membrane IgE. In these mice, GFP expression marks IgE cells, and a population of IgG1 cells with a rearrangement to Cepsilon in the non-productive (VDJ negative) IgH chromosome.

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Transcriptomics of BCR-stimulated IgG1 and IgG4 human B cell clones

Project description:We characterize the transcriptomic profile of a set of human IgG1 and IgG4-switched memory B cell clones

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IgG1 Immune Complexes Inhibit Naïve T Cell Proliferation but Stimulate a Subset of Their Progeny

Project description:We examined the effects of well-defined, soluble IgG1 immune complexes on the phenotypes of human peripheral naive CD8+ T cells. We demonstrate that IgG1-ICs inhibit the proliferation and differentiation of one subset of naïve T cells but stimulate the division of another naïve-like subset. We utilize RNA-Seq to characterize the inhibited and stimulated T cell subsets.

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Analysis of IgG1 producing CHO cells

Project description:The effects of changes in bioprocessing parameters (temp, pH, DO) on anti-IL8 IgG1 producing Chinese hamster ovary (CHO) cells were studied on the level of host cell proteome expression using TMT-SPS-MS3.

2021-04-09 | PXD017779 | Pride

ApoE determines the metabolic fate of apoC-III

Project description:Hypertriglyceridemia results from accumulation of triglyceride (TG)-rich lipoproteins (TRLs) in the circulation and is associated with increased cardiovascular disease risk. ApoC-III is an apolipoprotein on TRLs and a prominent negative regulator of TG catabolism. We recently established that in vivo apoC-III predominantly inhibits LDLR and LRP1 mediated hepatic TRL clearance and that apoC-III enriched TRLs are preferentially cleared by syndecan-1 (SDC1). In this study, we determined the impact of apoE, a common ligand for all three receptors, on apoC-III metabolism using apoC-III antisense oligonucleotide (ASO) treatment in mice lacking apoE and functional SDC1 (Apoe(-/-) Ndst1(f/f) Alb-Cre+). ApoC-III ASO treatment significantly reduced plasma TG levels in Apoe(-/-) Ndst1(f/f) Alb-Cre+ mice without reducing hepatic VLDL production or improving hepatic TRL clearance. Further analysis revealed that apoC-III ASO treatment lowered plasma TGs in Apoe(-/-) Ndst1(f/f) Alb-Cre+ mice, which was associated with increased LPL activity in white adipose tissue (WAT) in the fed state. Finally, clinical data confirm that ASO-mediated lowering of apoC-III via volanesorsen can reduce plasma TG levels independent of the apoE isoform genotype. Our data indicate that apoE determines the metabolic impact of apoC-III as we establish that apoE is essential to mediate inhibition of TRL clearance by apoC-III and that in the absence of functional apoE apoC-III inhibits tissue LPL activity.

2019-05-24 | GSE131284 | GEO

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