Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Analysis of gene expression in different T cell clones

ABSTRACT: The aim was to analyze the expression of genes in T cell clones having different functional profiles (Th1, Th0, Th17, Th2) obtained from the same individual. Keywords: Gene expression, T cell clones, Th17 characterisation The T cell clones were derived according to well known protocol, using different cytokines, and classified on the basis of their ability to produce cytokines. Once characterized for their production of IL-4, IL-12, gamma-IFN, IL-13, IL-1, they were used to prepare microarray experiments.

ORGANISM(S): Homo sapiens

SUBMITTER: Raffaele De Palma

PROVIDER: E-GEOD-11553 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Human interleukin 17-producing cells originate from a CD161+CD4+ T cell precursor.

Cosmi Lorenzo L De Palma Raffaele R Santarlasci Veronica V Maggi Laura L Capone Manuela M Frosali Francesca F Rodolico Gabriella G Querci Valentina V Abbate Gianfranco G Angeli Roberta R Berrino Liberato L Fambrini Massimiliano M Caproni Marzia M Tonelli Francesco F Lazzeri Elena E Parronchi Paola P Liotta Francesco F Maggi Enrico E Romagnani Sergio S Annunziato Francesco F

The Journal of experimental medicine 20080728 8

We demonstrate that CD161 is a highly up-regulated gene in human interleukin (IL) 17 T helper cell (Th17) clones and that all IL-17-producing cells are contained in the CD161(+) fraction of CD4(+) T cells present in the circulation or in inflamed tissues, although they are not CD1-restricted natural killer T cells. More importantly, we show that all IL-17-producing cells originate from CD161(+) naive CD4(+) T cells of umbilical cord blood, as well as of the postnatal thymus, in response to the c ...[more]

PMID: 18663128

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Project description:How signals from fatty acid metabolism are translated into changes in food intake remains unclear. Previously we reported that mice with a genetic inactivation of Acads (short-chain acyl-CoA dehydrogenase), encoding the enzyme responsible for mitochondrial beta-oxidation of C4-C6 short-chain fatty acids (SCFAs), shift consumption away from fat and toward carbohydrate when offered a choice. This finding demonstrated that the loss of a specific enzyme in fatty acid oxidation alters the choice of diet intake. To our knowledge, there are no reports of studies on the effects of dietary fat on the brain transcriptome in genetic models of fatty acid oxidation deficiency. The current study aimed to identify molecular mediators underlying the effects of SCFA oxidation deficiency on food intake. The current study aimed to identify molecular mediators underlying the effects of SCFA oxidation deficiency on food intake. We performed a transcriptional screen for gene expression in brain tissue of Acads-/- and Acads+/+ mice fed either high-fat (HF) or low-fat (LF) diet for 2 d. Ingenuity Pathway Analysis revealed three top-scoring pathways significantly modified by genotype or diet: oxidative phosphorylation, mitochondrial dysfunction, and CREB signaling in neurons. A comparison of statistically significant responses in HF Acads-/- vs. HF Acads+/+ (3917) and Acads+/+ HF vs. LF Acads+/+ (3879) revealed 2551 genes or approximately 65% in common between the two experimental comparisons. All but one of these genes were expressed in opposite direction with similar magnitude, demonstrating that Acads-deficient mice fed HF diet display transcriptional responses that mimic those of wildtype Acads+/+ mice fed LF diet. Intriguingly, genes involved in energy sensing and metabolism followed this pattern. Quantitative RT-PCR in hypothalamus confirmed the dysregulation of several genes in these pathways. Western blotting showed that the combination of Acads deficiency and HF diet increased hypothalamic AMP-kinase, a key protein in an energy-sensing cascade that responds to depletion of ATP. Our results suggest that the decreased beta oxidation of short-chain fatty acids in Acads-deficient mice fed HF diet produces a state of energy deficiency in the brain and that AMP-kinase is the cellular energy-sensing mechanism linking fatty acid oxidation to feeding behavior in this model. Twelve-week old male BALB/cByJ (Acads-/-) and BALB/cByKZ (Acads+/+) mice were fed a high-fat (D12331; Research Diets) and low-fat (D12329) diet for two days. Total RNA from whole brain tissue was obtained from three mutant (Acads-/-) and three wild-type (Acads+/+) mice of each diet group. All mice had similar body weights before diets were initiated. Gene expression in brain was compared between strains and between diets. Twelve-week old male BALB/cByJ (Acads-/-) and BALB/cByKZ (Acads+/+) mice were fed a high-fat (D12331; Research Diets) and low-fat (D12329) diet for two days. Total RNA from liver was obtained from three mutant (Acads-/-) and three wild-type (Acads+/+) mice of each diet group. All mice had similar body weights before diets were initiated. Gene expression in liver was compared between strains and diets.

Dataset Information

Analysis of gene expression in different T cell clones

Publications

Human interleukin 17-producing cells originate from a CD161+CD4+ T cell precursor.

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