Project description:scRNAseq of in vitro polarized Th17 and Th22 cells (Gpr65_WT versus KO), to compare metabolism gene expression in Gpr65_WT versus KO.
Project description:Microarray was used to delineate the global gene expression profile underlying the specific developmental program of two divergent antigen-specific T helper subsets (Th22 versus Th17) by identifying upregulation or downregulation of key lineage-determining transcription factors, cytokines, chemokines and other genes that govern their functional attributes. To identify factors that might distinguish the Th22 and Th17 developmental programs, comparative global transcriptome analysis between these 2 subsets was performed. Naïve splenic CD4+ T cells from OT-II-transgenic mice were isolated and grown in vitro under T-helper lineage-specific conditions in the presence of cognate antigen (ovalbumin) to identify their distinctive global gene-regulation profiles.
Project description:Microarray was used to delineate the global gene expression profile underlying the specific developmental program of two divergent antigen-specific T helper subsets (Th22 versus Th17) by identifying upregulation or downregulation of key lineage-determining transcription factors, cytokines, chemokines and other genes that govern their functional attributes.
Project description:In this study, we aimed to elucidate the profile of lesional and non-lesional keloid skin compared to normal skin. We performed gene (RNAseq, qRT-PCR) and protein (immunohistochemistry) expression analyses on biopsy specimens obtained from lesional and non-lesional skin of African American (AA) keloid patients compared to healthy skin from AA controls. We found that lesional versus normal skin showed significant up-regulation of markers of T-cell activation/migration (ICOS, CCR7), Th2- (IL-4R, CCL11, TNFSF4/OX40L), Th1- (CXCL9/CXCL10/CXCL11), Th17/Th22- (CCL20, S100As) pathways, and JAK/STAT-signaling (JAK3) (false-discovery rate [FDR]<0.05).
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:Single cell RNAseq from brain endothelial cells (BECs) isolated from wild-type and Iqgap2-/- (KO) mice to identify transcriptional changes in BECs caused by loss of Iqgap2. Mouse brains were dissociated to single cell suspension and labelled with CD31. CD31+ cells were flow sorted and processed for single cell RNAseq.
Project description:RNAseq was performed by to compare gene expression between wildtype and Smchd1 KO ES cells, the gene expression pattern in Dux KO mutants , Double KO mutant Tet-TKO mutants and Tet TKO plus SMCKHD1 KO mutants were analyzed by RNAseq.
Project description:Dysregulation of CD4+ T cell populations leads to intestinal inflammation, but the regional differences of these T cell populations remained unclear in the healthy population. We first used flow cytometry to show that Th17 and Th22 cells are specifically enriched in the human cecum, while Th1 and Th2 cells do not differ regionally. We subsequently performed transcriptional profiling and found that Th17 was positively associated with the expression of RETN and negatively associated with TFF1, suggesting that the differential enrichment of Th17 cells in the healthy human cecum was underlined by the metabolic differences in this environment. Transcriptional profiling with microarray on human intestinal pinch biopsies obtained from different sites of the healthy colon.