Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

S mansoni infection B cell comparison

ABSTRACT: The helminth Schistosoma Mansoni is known to generate a regulatory B cell population that can suppress in multiple murine experimental models. Microarray comparison allows for a greater understanding as to how these cells are generated and their implications in immune regulation.

ORGANISM(S): Mus musculus

SUBMITTER: Fallon Padraic

PROVIDER: E-MTAB-2100 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Regulatory B cells prevent and reverse allergic airway inflammation via FoxP3-positive T regulatory cells in a murine model.

Amu Sylvie S Saunders Sean P SP Kronenberg Mitchell M Mangan Niamh E NE Atzberger Ann A Fallon Padraic G PG

The Journal of allergy and clinical immunology 20100320 5

<h4>Background</h4>Parasitic helminth infections of humans have been shown to suppress the immune response to allergens. Experimentally, infection of mice with the helminth Schistosoma mansoni prevents allergic airway inflammation and anaphylaxis via IL-10 and B cells.<h4>Objective</h4>To identify and characterize the specific helminth-induced regulatory B-cell subpopulation and determine the mechanism by which these regulatory B cells suppress allergic airway inflammation.<h4>Methods</h4>IL-10- ...[more]

PMID: 20304473

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Project description:Background: Global DNA methylation contributes to genomic integrity by supressing repeat associated transposition events. Several chromatin factors are required in addition to DNA methyltransferases to maintain DNA methylation at intergenic and satellite repeats. Embryos lacking Lsh, a member of the SNF2 superfamily of chromatin helicases, are hypomethylated. The interaction of Lsh with the de novo methyltransferase, Dnmt3b, facilitates the deposition of DNA methylation at stem cell genes. We wished to determine if a similar targeting mechanism operates to maintain DNA methylation at repetitive sequences. Results: We used HELP-seq to map genome wide DNA methylation patterns in Lsh-/- and Dnmt3b-/- somatic cells. DNA methylation is predominantly lost from specific genomic repeats in Lsh-/- cells: LTR-retrotransposons, LINE-1 repeats and mouse satellites. RNA-seq experiments demonstrate that specific IAP (Intracisternal A-type particle) LTRs and satellites, but not LINE-1 elements, are aberrantly transcribed inLsh-/- cells. LTR hypomethylation in Dnmt3b-/- cells is moderate and hypomethylated repetitive elements (IAP, LINE-1 and satellite) are silent. Chromatin immunoprecipitation (ChIP) indicates that repressed LINE-1 elements gain H3K4me3, but H3K9me3 levels are unaltered in Lsh-/- cells, indicating that DNA hypomethylation alone is not permissive for their transcriptional activation. Mis-expressed IAPs and satellites lose H3K9me3 and gain H3K4me3 in Lsh-/- cells. Conclusions: Our study emphasizes that regulation of repetitive elements by DNA methylation is selective and context dependent. We propose a model where Lsh is specifically required at a precise developmental window to target de novo methylation to repeat sequences, which is subsequently maintained by Dnmt1 in somatic cells to enforce repeat silencing thus contributing to genomic integrity. Two pairs of genomic samples compared: WT and Lsh-/- DNA isolations from tail-tip fibroblasts; WT and Dnmt3b knockout DNA isolations from mouse embryonic fibroblasts.

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Dataset Information

S mansoni infection B cell comparison

Publications

Regulatory B cells prevent and reverse allergic airway inflammation via FoxP3-positive T regulatory cells in a murine model.

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