Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Autoregulation of Th1-mediated inflammation by twist1

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE11556 | GEO | 2008/05/24

SECONDARY ACCESSION(S): PRJNA106287

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Autoregulation of Th1-mediated inflammation by twist1.

Project description: Not available

| S-EPMC2525589 | biostudies-literature

Transcription profiling of mouse splenic thymocytes reveals autoregulation of Th1-mediated inflammation by twist1

Project description:This SuperSeries is composed of the following subset Series:; GSE11533: Autoregulation of Th1-mediated inflammation by twist1 1st part; GSE11534: Autoregulation of Th1-mediated inflammation by twist1 2nd part Experiment Overall Design: Refer to individual Series

2008-06-18 | E-GEOD-11556 | biostudies-arrayexpress

Architecture of Epigenetic Reprogramming Following Twist1 Mediated Epithelial-Mesenchymal Transition

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-12-10 | E-GEOD-53026 | biostudies-arrayexpress

Autoregulation of Th1-mediated inflammation by twist1 1st part

Project description:The basic helix-loop-helix transcriptional repressor twist1, as an antagonist of nuclear factor κB (NF-κB)-dependent cytokine expression, is involved in the regulation of inflammation-induced immunopathology. We could show that twist1 is expressed by activated T helper (Th) 1 effector memory cells. Induction of twist1 in Th cells is dependent on NF-κB, nuclear factor of activated T cells (NFAT), and interleukin (IL)-12 signaling via signal transducer and activator of transcription (STAT) 4. Expression of twist1 is transient following T-cell receptor engagement, and increases upon repeated stimulation of Th1 cells. Imprinting for enhanced twist1 expression is characteristic of repeatedly restimulated effector memory Th cells and thus of the pathogenic memory Th cells of chronic inflammation. Th lymphocytes from the inflamed joint or gut tissue of patients with rheumatic diseases, Crohn’s disease or ulcerative colitis express high levels of twist1. Expression of twist1 in Th1 lymphocytes limits the expression of the cytokines interferon-γ, IL-2 and tumor necrosis factor-α, and ameliorates Th1-mediated immunopathology in delayed-type hypersensitivity and antigen-induced arthritis. In order to identify the effect of twist1 expression on the function of Th cells, twist1 was ectopically expressed and the transcriptome was compared to empty-virus infected control cells. In addition, this experiment allows for the identification of genes regulated by the transcription factor twist1.

2008-05-24 | GSE11533 | GEO

Autoregulation of Th1-mediated inflammation by twist1 2nd part

Project description:Gene expression profiling of repeatedly activated compared to recently activated Th1 cells to identify genes that play a role in chronic inflammatory disorders and may qualify as diagnostic or therapeutic targets; Upon activation under appropriate costimulatory conditions, naive T helper (Th) cells differentiate into Th2 or Th17 cells, each characterized by the expression of specific effector cytokines. In response to a repeated stimulation with antigen, Th cells develop a stable memory for the expression of those cytokines as well as for other secreted or membrane-associated factors. The stable memory for the expression of proinflammatory effector functions may explain the resistance of Th effector cells to conventional immunosuppressive therapy, and the inability of immunosuppression to cure chronic inflammation. The imprinting of the functional memory is based on epigenetic modifications and expression of distinct transcription factors. In this project, we compare the transcriptomes of once and repeatedly activated murine Th1 cells, to identify genes that induce and maintain the functional memory and control the persistence of pathogenic memory Th1 cells. This in turn might help to discriminate pathogenic versus protective cells in immunopathology and present novel targets for the diagnosis and therapy of chronic inflammatory disease.

2008-05-24 | GSE11534 | GEO

Inflammation-Driven Carcinogenesis is Mediated through STING

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-05-31 | E-GEOD-57605 | biostudies-arrayexpress