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Premature activation of immune transcription programs in autoimmune-predisposed mouse embryonic stem cells and blastocysts

ABSTRACT: To study the underlying mechanism of autoimmunity predisposition in autoimmune-prone mouse strains, we characterize embryonic stem cells derived from various mouse strains.

ORGANISM(S): Mus musculus

PROVIDER: GSE155045 | GEO | 2020/08/11

REPOSITORIES: GEO

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Premature activation of immune transcription programs in autoimmune-predisposed mouse embryonic stem cells and blastocysts

Project description:To study the underlying mechanism of autoimmunity predisposition in autoimmune-prone mouse strains, we characterize embryonic stem cells derived from various mouse strains.

2020-08-11 | GSE154458 | GEO

Premature activation of immune transcription programs in autoimmune-predisposed mouse embryonic stem cells and blastocysts

Project description:To study the underlying mechanism of autoimmunity predisposition in autoimmune-proned mouse strains, we characterize embryonic stem cells derived from various mouse strains.

2020-08-11 | GSE155044 | GEO

Premature Activation of Immune Transcription Programs in Autoimmune-Predisposed Mouse Embryonic Stem Cells and Blastocysts.

Project description:Autoimmune diabetes is a complex multifactorial disease with genetic and environmental factors playing pivotal roles. While many genes associated with the risk of diabetes have been identified to date, the mechanisms by which external triggers contribute to the genetic predisposition remain unclear. Here, we derived embryonic stem (ES) cell lines from diabetes-prone non-obese diabetic (NOD) and healthy C57BL/6 (B6) mice. While overall pluripotency markers were indistinguishable between newly derived NOD and B6 ES cells, we discovered several differentially expressed genes that normally are not expressed in ES cells. Several genes that reside in previously identified insulin-dependent diabetics (Idd) genomic regions were up-regulated in NOD ES cells. Gene set enrichment analysis showed that different groups of genes associated with immune functions are differentially expressed in NOD. Transcriptomic analysis of NOD blastocysts validated several differentially overexpressed Idd genes compared to B6. Genome-wide mapping of active histone modifications using ChIP-Seq supports active expression as the promoters and enhancers of activated genes are also marked by active histone modifications. We have also found that NOD ES cells secrete more inflammatory cytokines. Our data suggest that the known genetic predisposition of NOD to autoimmune diabetes leads to epigenetic instability of several Idd regions.

| S-EPMC7460978 | biostudies-literature

Premature activation of immune transcription programs in autoimmune-predisposed mouse embryonic stem cells and blastocysts

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-08-11 | GSE155046 | GEO

Premature activation of immune transcription programs in autoimmune-predisposed mouse embryonic stem cells and blastocysts

Project description:Premature activation of immune transcription programs in autoimmune-predisposed mouse embryonic stem cells and blastocysts

| PRJNA648339 | ENA

Premature activation of immune transcription programs in autoimmune-predisposed mouse embryonic stem cells and blastocysts

Project description:Premature activation of immune transcription programs in autoimmune-predisposed mouse embryonic stem cells and blastocysts

| PRJNA646374 | ENA

Premature activation of immune transcription programs in autoimmune-predisposed mouse embryonic stem cells and blastocysts

Project description:Premature activation of immune transcription programs in autoimmune-predisposed mouse embryonic stem cells and blastocysts

| PRJNA648343 | ENA

Premature activation of immune transcription programs in autoimmune-predisposed mouse embryonic stem cells and blastocysts

Project description:Premature activation of immune transcription programs in autoimmune-predisposed mouse embryonic stem cells and blastocysts

| PRJNA648327 | ENA

Sex Bias in CNS Autoimmune Disease Mediated by Androgen Control of Autoimmune Regulator

Project description:Male gender is protective against multiple sclerosis and other T cell-mediated autoimmune diseases. This protection may be due, in part, to higher androgen levels in males. Androgen binds to the androgen receptor (AR) to regulate gene expression, but how androgen protects against autoimmunity is not well-understood. Autoimmune Regulator (Aire) prevents autoimmunity by promoting self-antigen expression in medullary thymic epithelial cells, such that developing T cells that recognize these self-antigens within the thymus undergo clonal deletion. Here, we show that androgen upregulates Aire-mediated thymic tolerance to protect against autoimmunity. Androgen recruits AR to Aire promoter regions, with consequent enhancement of Aire transcription. In mice and humans, thymic Aire expression is higher in males compared to females. Androgen administration and male gender protect against autoimmunity in a multiple sclerosis mouse model in an Aire-dependent manner. Thus, androgen control of an intrathymic Aire-mediated tolerance mechanism contributes to gender differences in autoimmunity. RNA-seq comparison of male vs. female expression in mTEC cells. Pools of 10 mice each were used for each replicate (two for male and two for female)

2016-03-09 | E-GEOD-79014 | biostudies-arrayexpress

The gut microbiome protects genetically predisposed mice against leukemia

Project description:We used microarrays to investigate gene expression changes in leukemic cells from Pax5+/- mice treated with antibiotics. Precursor B cell acute lymphoblastic leukemia (pB-ALL), the most common type of childhood leukemia, is frequently characterized by the cooperation of a genetic predisposition acquired in utero and secondary oncogenic events taking place only in a fraction of predisposed children after birth. Although predisposition can be detected at birth, it is currently unknown which factors determine the development of overt leukemia in genetic carriers and how this can be potentially prevented. Experimental studies have shown that infectious stimuli promote disease onset in genetically predisposed mice. Here, we analyzed the impact of the microbiome on leukemogenesis in a mouse model (Pax5+/- mice) that faithfully mimicks genetic predisposition and leukemogenesis of human pB-ALL related to the synergy of genetic predisposition and exposure to a natural infectious environment. Employing 16S rRNA sequencing and machine learning we can accurately predict a distinct gut microbiome which is determined by a specific constitutional genetic variant. Deprivation of the gut microbiome by antibiotic treatment enhanced pB-ALL development in Pax5+/- predisposed (63% vs. 22%) but not in wildtype mice (0%). This finding was observed in the presence but also -to a lesser extent- in the absence of a natural, infectious environment (48%). The composition of the gut microbiome constitutes a biomarker signature and allows to identify specifically those Pax5+/- mice that developed leukemia. This indicates that the gut microbiome can be used to identify carriers at risk to develop leukemia and to reduce this risk by early-life interventions.

2019-10-30 | GSE139547 | GEO

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