Project description:To detect the miRNA expression profile in CCR6+ regulatory T cells In this study, the total RNA was extracted from CCR6+ regulatory T cells and CCR6- regulatory T cells. Then, the expression profile of miRNA on these cells was detected by microarray.
Project description:Backgroud. CCR6(+) CD4(+) regulatory T cells (CCR6(+) Tregs), a distinct Tregs subset, played an important role in various immune diseases. Recent evidence showed that microRNAs (miRNAs) are vital regulators in the function of immune cells. However, the potential role of miRNAs in the function of CCR6(+) Tregs remains largely unknown. In this study, we detected the expression profile of miRNAs in CCR6(+) Tregs. Materials and Methods. The expression profile of miRNAs as well as genes in CCR6(+) Tregs or CCR6(-) Tregs from Balb/c mice were detected by microarray. The signaling pathways were analyzed using the Keggs pathway library. Results. We found that there were 58 miRNAs significantly upregulated and 62 downregulated up to 2 fold in CCR6(+) Tregs compared with CCR6(-) Tregs. Moreover, 1,391 genes were observed with 3 fold change and 20 signaling pathways were enriched using the Keggs pathway library. Conclusion. The present data showed CCR6(+) Tregs expressed specific miRNAs pattern, which provides insight into the role of miRNAs in the biological function of distinct Tregs subsets.
Project description:Chemokine receptor CCR6 is a G-protein-coupled receptor that binds its high-affinity ligand, CCL20. Among the CD4+ T cells, Th17 and regulatory T cells express CCR6, which facilitates their migration in CCL20-enriched, inflamed tissue. Migration of CCR6+ T cells from secondary lymphoid tissues into inflamed tissues exposes them to a distinct metabolic microenvironment. What drives the metabolic adaptation of cells in these tissues and what contributes to their effector or regulatory function is not clearly understood. During colitis, increased gut production of CCL20 promotes the recruitment of these cells. We demonstrated that the intrinsic signaling of CCL20-CCR6 in CD4+ T cells promotes the differentiation of inflamatory Th1-like Th17 cells (T-bet+RORγt+) during colitis in both mouse models and humans. This signaling induces rapamycin-sensitive phosphorylation of PI3K, Akt, mTORC1, and STAT3 in a CCR6-dependent manner. RNA-seq and proteomics analysis revealed alterations in CCL20 during Th17 differentiation, affecting several metabolic pathways, including energy metabolism. CCL20 significantly increased glycolysis and inhibited oxidative phosphorylation, thereby driving the differentiation of pathogenic Th17 cells. Our findings suggest that alterations in CCR6-induced changes in Th17 metabolism offer an interesting therapeutic target for gut inflammation and autoimmunity.
Project description:To study the miRNA modulating network and different expressed miRNA lists in prostate cancer, we use high-throughout method to genomically detect the expression profile of miRNA, mRNA and protein.
Project description:Microarrays were used to determine transcriptional differences between CCR6+ ILC3s isolated from RorccreTnfsf11fl/fl and Tnfsf11fl/fl small intestine lamina propria.
Project description:Microarray was used to determine transcriptional differences between Nr1d1+/+ CCR6+ ILC3s and Nr1d1-/- CCR6+ ILC3s isolated from small intestine lamina propria