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Transcriptome analysis of Th9 CD4+ T cells differentiated with or without Il-1beta

ABSTRACT: We report that the Th9 differenciation program is boosted in presence of Il-1beta

ORGANISM(S): Mus musculus

PROVIDER: GSE54697 | GEO | 2014/05/23

SECONDARY ACCESSION(S): PRJNA237440

REPOSITORIES: GEO

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Transcriptome analysis of Th9 CD4+ T cells differentiated with or without Il-1beta

Project description:We report that the Th9 differenciation program is boosted in presence of Il-1beta Examination of the expression profile of Th9 CD4+ T cells after 1 hour and 3 days of differentiation and after in vivo injection

2014-05-23 | E-GEOD-54697 | biostudies-arrayexpress

Transcriptome analysis of CD4+ T cells differentiated from wild-type and CD4cre IRF8flox mice

Project description:We report that the Th9 differenciation program is alterated in absence of IRF8 protein

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Project description:We report that the IRF8 protein is able to interact with chromatin during Th9 differenciation

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Effect of IL-7 on CD4+ T cell and Th9 cells

Project description:We found that IL-7 pretreatment enhanced Th9 differentiation. To clarify the underlying mechanisms, we examine the gene expression profiles of CD4+ T cell and Th9 cells with or without IL-7 pretreatment. In Th9 cells, we found that Th9 related genes were greatly increased in IL-7 Th9 group, which demonstrated an enhanced Th9 differentiation. In CD4+ T cells, we found that IL-7 treatment resulted in a global gene expression change especially on chromatin remodeling related genes, which facilitated the entry of transcriptional factor to the Il9 promoter region and promoted Il9 transcription.

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2016-08-01 | E-GEOD-60320 | biostudies-arrayexpress

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Project description:Microarray analyses were performed to compare gene expression in cultured mouse Th9, Th2 and Treg cells and resting versus activated Th9 cells. Three replicates were analyzed for each culture condition; Th9 unstim, Th2 unstim, Treg unstim, Th9 stim

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Rat primary chondrocyte: Control vs. IL-1beta treated

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Opposing actions of IL-2 and IL-21 on Th9 differentiation correlate with their differential regulation of BCL6 expression

Project description:Interleukin 9 (IL-9) is a γc-family cytokine that is highly produced by T-helper 9 (Th9) cells and regulates a range of immune responses, including allergic inflammation. Here we show that IL-2–JAK3–STAT5 signaling is required for Th9 differentiation, with critical STAT5 binding sites in the Il9 (the gene encoding IL-9) promoter. IL-2 also inhibited B cell lymphoma 6 (BCL6) expression, and over- expression of BCL6 impaired Th9 differentiation. In contrast to IL-2, IL-21 induced BCL6 and diminished IL-9 expression in wild-type but not Bcl6−/− cells, whereas Th9 differentiation was increased in Il21−/− or Il21r−/− T cells. Interestingly, BCL6 bound in proximity to many STAT5 and STAT6 binding sites, including at the Il9 promoter. Moreover, there was increased BCL6 and decreased STAT binding at this site in cells treated with blocking antibodies to IL-2 and the IL-2 receptor, suggesting a possible BCL6–STAT5 binding competition that influences IL-9 production. BCL6 binding was also increased when cells were Th9-differentiated in the presence of IL-21. Thus, our data reveal not only direct IL-2 effects via STAT5 at the Il9 gene, but also opposing actions of IL-2 and IL-21 on BCL6 expression, with increased BCL6 expression inhibiting IL-9 production. These data suggest a model in which increasing BCL6 expression decreases efficient Th9 differentiation, indicating possible distinctive approaches for controlling this process. Genome-wide transcription factors mapping and binding of STAT5B and STAT6 in mouse polarized Th9 cells treated with or without blocking antibodies to IL-2 (anti-IL-2). RNA-Seq is conducted in WT and Il2-/- mice.

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