ND and HFD memory phenotype CD4 T cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE70472 | GEO | 2015/07/02
SECONDARY ACCESSION(S): PRJNA288764
REPOSITORIES: GEO
Similar Datasets
Project description:We used microarray analysis to identify specific molecular mechanisms controlling Th17 cell differentiation in HFD mice Memory phenotype CD4 T cells derived from ND or HFD mice were selected for RNA extraction and hybridization on Affymetrix microarrays.
2015-07-02 | E-GEOD-70472 | biostudies-arrayexpress
Project description:Carbo2013 - Cytokine driven CD4+ T Cell differentiation and phenotype plasticity
CD4+ T cells can differentiate into different phenotypes
depending on the cytokine milieu. Here a computational and mathematical model with sixty ordinary differential equations representing a CD4+ T cell differentiating into either Th1, Th2, Th17 or iTreg cells, has been constructed.
The model includes cytokines,
nuclear receptors and transcription factors that define fate
and function of CD4+ T cells. Computational simulations
illustrate how a proinflammatory Th17 cell can undergo
reprogramming into an anti-inflammatory iTreg phenotype
following PPARc activation.
This model is described in the article:
Systems Modeling of Molecular Mechanisms Controlling Cytokine-driven CD4+ T Cell Differentiation and Phenotype Plasticity.
Carbo A, Hontecillas R, Kronsteiner B, Viladomiu M, Pedragosa M, Lu P, Philipson CW, Hoops S, Marathe M, Eubank S, Bisset K, Wendelsdorf K, Jarrah A, Mei Y, Bassaganya-Riera J
PLoS Computational Biology [2013, 9(4):e1003027]
Abstract:
Differentiation of CD4+ T cells into effector or regulatory phenotypes is tightly controlled by the cytokine milieu, complex intracellular signaling networks and numerous transcriptional regulators. We combined experimental approaches and computational modeling to investigate the mechanisms controlling differentiation and plasticity of CD4+ T cells in the gut of mice. Our computational model encompasses the major intracellular pathways involved in CD4+ T cell differentiation into T helper 1 (Th1), Th2, Th17 and induced regulatory T cells (iTreg). Our modeling efforts predicted a critical role for peroxisome proliferator-activated receptor gamma (PPARγ) in modulating plasticity between Th17 and iTreg cells. PPARγ regulates differentiation, activation and cytokine production, thereby controlling the induction of effector and regulatory responses, and is a promising therapeutic target for dysregulated immune responses and inflammation. Our modeling efforts predict that following PPARγ activation, Th17 cells undergo phenotype switch and become iTreg cells. This prediction was validated by results of adoptive transfer studies showing an increase of colonic iTreg and a decrease of Th17 cells in the gut mucosa of mice with colitis following pharmacological activation of PPARγ. Deletion of PPARγ in CD4+ T cells impaired mucosal iTreg and enhanced colitogenic Th17 responses in mice with CD4+ T cell-induced colitis. Thus, for the first time we provide novel molecular evidence in vivo demonstrating that PPARγ in addition to regulating CD4+ T cell differentiation also plays a major role controlling Th17 and iTreg plasticity in the gut mucosa.
Author's comment:
CD4+ T cell computational model (Version 1.4)
Steady state corrected. There was a problem in the internalization of IL-17 in its mathematical function.
This model is hosted on BioModels Database
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To the extent possible under law, all copyright and related or
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2024-09-02 | BIOMD0000000451 | BioModels
Project description:In this study we want to compare the gene expression profile of CD44+CXCR6+ CD8+ T cells from the liver of ND and CD-HFD mice with hepatic CD44+CXCR6neg and splenic CD44+ CX3CR1neg CD8 T cells of ND and CD-HFD mice. This comparison will reveal transcriptional signatures of hepatic CD44+CXCR6+ CD8+ T cells in CD-HFD responsible for causing liver pathology in NASH.
2020-12-18 | GSE145104 | GEO
Project description:To investigate the effects of a high-fat diet (HFD) on the skin, RNA-seq was performed on the ear skin after 8 weeks of normal diet (ND) and HFD-fed mice. We also examined the effects of a HFD on irritant dermatitis by PMA.
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Project description:Transcriptional profiling for screening olfactory receptor expressions in C57BL/6J mouse liver and adipose tissue under either ND and HFD
2017-08-24 | GSE102977 | GEO
Project description:Pyrosequencing analysis of microbial communities of mice fed normal diet (ND), high fat diet (HFD) or HFD supplemented with KFLAB (HFD-KFLAB) using 454 GS FLX Titanium System
| PRJEB2698 | ENA
Project description:Purpose: Aim of the study is to identify changes in hepatic gene expression induced by either a 40kcal% coconut oil rich high fat diet (HFD), a 40kcal% soybean oil plus coconut oil high fat diet (SO-HFD) or a low fat vivarium chow diet (Viv). Methods: Livers from mice that had been fed one of the above mentioned diets for 35 weeks, were used to make cDNA libraries that were then sent for deep sequencing, using the Illumina TruSeq RNA. Result: Many genes involved in metabolism, lipid binding, transport and storage and many Cyp genes are dysregulated in the two high fat diets as compared to Viv HFDs in SO-HFD mice. Comparing the two HFDs shows more metabolism and disease related genes dysregulated in SO-HFD vs HFD. Conclusion: A diet high in soybean oil may be more detrimental to metabolic health than a diet high in saturated fats. cDNA isolated from livers from mice fed HFD, SO-HFD or Viv for 35 weeks, were 50bp pair-ended sequenced in triplicate using Illumina TruSeq RNA Sample Prep v2 Kit.
2015-08-28 | E-GEOD-68360 | biostudies-arrayexpress
Project description:Microarray data, 4 week HFD/NCD, nostim or 16hrstim
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Project description:In latent tuberculosis infection (LTBI) spread of the bacteria is contained by a persistent immune response, which includes CD4+ T cells as important contributors. Here we show that TB-specific CD4+ T cells have a characteristic chemokine expression signature (CXCR3+CCR6+CCR4-; Th* cells), and that the overall number of Th* cells is significantly increased in LTBI donors. We have comprehensively characterized the transcriptional signature of Th* cells and find significant differences to conventional Th1, Th17 and Th2 cells, but no major changes between healthy and LTBI donors. Th* cells display linage-specific signatures of both Th1 and Th17 cells, but also have a unique gene expression program including genes associated with susceptibility to TB, enhanced T cell activation, enhanced cell survival, and induction of a cytotoxic program akin to CTL cells. Overall, the gene expression signature of Th* reveals characteristics of cells important in controlling latent infections.
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