Project description:To investigate the effect of pemafibrate to Th17 cells, we differentiated naive T cells under Th17 condition. We then performed gene expression profiling analysis using data obtained from RNA-seq of 2 groups at 48hr after polarization.
Project description:The early stages of human Th17 Cell differentiation were studied using label free proteomics to compare Th17 polarized CD4+ human T cells at 24 h and 72 h with activated cells (72 and 24 h) and Thp cells.
Project description:Transcriptional profiling of T-cells isolated from spleen of IRF4 -/- mice and cultured under Th17 polarizing conditions for 42 hrs compared to cells similarly isolated and cultured from spleen of IRF4 +/- mice. The aim of the study was to identify global misexpression of genes in IRF4 -/- cells and hence identify key pathways regulated by IRF4 during Th17 differentiation. Two-condition experiment, IRF4 -/- vs IRF4 +/- Th17 cells at 42hrs. Biological replicates: 3 for each condition
Project description:Interleukin 17 (IL-17) producing T helper 17 (Th17) cells are critical drivers of pathogenesis in a variety of autoimmune and inflammatory diseases. Strategies to mitigate excessive Th17 response thus remain an attractive target for immunotherapies. Here we report that Cancerous Inhibitor of Protein Phosphatase 2A (CIP2A) regulates IL-17 production by Th17 cells in human and mouse. Using CIP2A knock-out (KO) mice and siRNA-mediated CIP2A silencing in human primary CD4+ T cells, we demonstrated that CIP2A silencing results in a significant increase in IL-17 production. Interestingly, CIP2A deficient Th17 cells were characterized by increased strength and duration of STAT3 (Y705) phosphorylation. Genome-wide gene expression profile as well as the p-STAT3 (Y705) interactome of CIP2A deficient Th17 cells identified that CIP2A regulates the strength of the interaction between Acylglycerol kinase (AGK) and STAT3, and thereby, modulates STAT3 phosphorylation as well as expression of IL-17 in Th17 cells. Our results uncover the physiological function of CIP2A in Th17 cells and provides new opportunities for therapeutic intervention in Th17 cell mediated diseases.
Project description:Th17 cells are implicated in autoimmune diseases and several metabolic processes are shown to be important for their development and function. However, the role of de novo sphingolipid biosynthesis in their differentiation and function is less known. To investigate the role of SPTLC1(major subunit of serine palmitoyl transferase enzyme (SPT) that catalyzes the first and rate limiting step of de novo sphingolipid synthesis) in mouse Th17 cell differentiation, we have activated the WT and SPTLC1 defecient (KO) naïve CD4+ T cells, isolated from mouse spleen and lymph nodes, in Th17 differentiating condition in the precence and absence of NAC ( N-acetyl cysteine) and 3-KDS (3-ketodihydrosphingosine).
Project description:We have shown that cathelicidin amplifies Th17 differentiation. To determine the mechanism through which this host defence peptide acts, we performed multiplex gene expression analysis (NanoString) to identify the effects of mouse cathelicidin (mCRAMP) on murine CD4+ T cells cultured under Th17-driving conditions.
Project description:In our previous work, we showed the positive effect of the magnesium and the negative effect of the copper on yeast fermentation performance. The magnesium increases the ethanol yield and a faster glucose consumption by the yeast, on the other hand, the copper provides an opposite effect in yeast under fermentation condition. Therefore, from this contrasting effect we performed the gene-wide expression analysis in the industrial yeast Saccharomyces cerevisiae JP1 under fermentation condition in order to reveal the gene expression profile upon magnesium and copper supplementation.