Project description:We report that Stat6-driven gene transcription regulates the transition from Tfh21 to Tfh4 cells, suppressing IL-21 production and promoting IL-4 secretion. We identified a cis-enhancer in the second intron of Il21 as a regulator of Tfh cell cytokine transition, via an effect of Stat6 on chromatin accessibility with repression of Il21 transcription. Chromatin accessibitiy of this second intron region was not affected in the naive CD4+ T cell population
Project description:Purpose: To examine the expression profile of WT and Stat6 KO intestinal stem cells. Methods: We isolated Lgr5+ ISCs from the intestine tissue, and generated Stat6 KO ISCs through CRISPR/Cas9 approach. Results: Many genes are changed upon Stat6 KO cells. We pay special attention on Wnt/β-catenin signaling that is the most critical pathway in ISCs, and discovered Stat6 drove the expression of Wnt target genes. Conclusions: Stat6 crosstalks with Wnt signaling to drive ISC self-renewal.
Project description:Gene expression data from wild-type and Bcl6-/- naive CD4 T cells In order to find genes regulated by Bcl6 in follicular helper T cells Naïve CD4 T cells were sorted from wild-type (WT) and T cell-specific conditional Bcl6-/- (KO) mice-- 8 samples, 4 WT and 4 KO
Project description:Gene expression data from wild-type and Bcl6-/- naive CD4 T cells In order to find genes regulated by Bcl6 in follicular helper T cells Naïve CD4 T cells were sorted from wild-type (WT) and T cell-specific conditional Bcl6-/- (KO) mice-- 8 samples, 4 WT and 4 KO
Project description:STAT6 is a major transcription factor driving the polarization of Th2 cells in response to cytokine IL-4. Here we have analyzed on a genome wide level the STAT6 mediated gene expression after IL-4 induction in naive human CD4+ T cells. RNAi mediated STAT6 knockdown was used to reveal the genes specifically regulated by STAT6. Total RNA from STAT6 siRNA treated cord blood CD4+ T cells 12, 24, 48 or 72 hours after culturing the cells in activating (antiCD3+antiCD28) plus or minus IL-4 conditions was compared to total RNA from nonspecific control siRNA treated cells. All together 18 samples were analyzed and 3 biological replicates of the culture were performed for a total of 54 samples.
Project description:We compared differences in fetal and adult T cells by performing whole genome profiling on sort-purified T cells (naïve CD4+ and Treg cells) from human fetal specimens (18-22 gestational weeks) and adult specimens (age 25-40 years old). Fetal and Adult Naïve CD4+ T cells phenotype: CD3+CD4+CD45RA+CCR7+CD27+, Fetal and Adult CD4+CD25+ Treg phenotype: CD3+CD4+CD25bright Four different groups were analyzed: Fetal Naïve CD4+ T cells, Adult Naïve CD4+ T cells, Fetal Treg cells, Adult Treg cells. For each group three independent donors were analyzed.
Project description:STAT6 is a major transcription factor driving the polarization of Th2 cells in response to IL-4. STAT6 is phosphorylated by Jak1 and Jak3 kinases at the IL-4 receptor, after which phosphorylated STAT6 forms a homodimer and translocates into the nucleus. There STAT6 binds to specific DNA sequences, regulating the transcription of its target genes. Here we have analyzed on a genome wide level the STAT6 binding sites, after 1h and 4h of IL-4 induction, in naive human CD4+ T cells. Keywords: SRA Altogether 5 samples from 1 biological replicate were analyzed. Activated and IL-4 treated samples were compared to only activated or untreated samples to identify unique STAT6 binding sites after IL-4 induction.
Project description:STAT6 is a major transcription factor driving the polarization of Th2 cells in response to cytokine IL-4. Here we have analyzed on a genome wide level the STAT6 mediated gene expression after IL-4 induction in naive human CD4+ T cells. RNAi mediated STAT6 knockdown was used to reveal the genes specifically regulated by STAT6.