ABSTRACT: This set features unfiltered, aligned, UMI-based single cell RNA sequencing count data for 5290 Blood, intraepithelial ileum (IEL) and lamina propria ileum (LPL) T cells from Crohn's disease patients as published in Uniken Venema et al, Gastroenterology 2019
Project description:We investigated the transcriptomic landscape of human CD8 tissue-resident T cells (Trm) derived from the ileum to study the differences in compartment (epithelium and lamina propria), CD103+ and CD103- Trm and inflammation-induced changes (active Crohn's disease vs healthy controls).
Project description:This scRNA-seq dataset of five human subjects with ulcerative colitis (derived from colonic lamina propria samples), was analyzed and published as part of a larger manuscript (Mitsialis, V et al, "“Single-Cell Analyses of Colon and Blood Reveal Distinct Immune Cell Signatures of Ulcerative Colitis and Crohn’s Disease” in Gastroenterology), which reported immune signatures of blood and intestinal tissue differentiating ulcerative colitis from Crohn's disease from non-IBD human subjects using mass cytometry as well as scRNA-seq.
Project description:In this project, we profiled small intestinal epithelium and lamina propria immune cells from 3-, 4-, 5- and 6-weeks old wild type (WT) littermate animals using 10X droplet based RNA sequencing of single cells. In the second part, we profiled small intestinal epithelium, lamina propria immune cells as well as intraepithelial immune cells from 5-weeks old WT mice derived from Jackson laboratories and littermate colonized with SFB (segmented filamentous bacteria) 2 weeks prior to analysis, using the same approach.
Project description:Crohn's disease (CD) is a chronic condition characterized by recurrent flares of inflammation of the gastrointestinal tract. Despite decades of research, the etiology of CD is poorly understood and is characterized by dysregulated immune activation that progressively destroys the gastrointestinal tissue. At the center of the pathology is the intestinal mucosa, where the epithelium and the lamina propria are main cellular compartments. While the epithelium contains predominantly epithelial cells, the lamina propria is enriched in immune cells and contains supporting stroma. Thus, the cells constituting these compartments can be classified as epithelial cells, immune cells and stromal cells. Gaining insight into how these cell types interact with each other is important to further our understanding of CD pathogenesis. Here, using isobaric labeling-based quantitative proteomics, we perform an exploratory study to analyze in-depth proteome changes in epithelial cells, immune cells and stromal cells purified by cell sorting from the intestinal mucosa of CD patients and controls. Our workflow preserving the link between the different cell types in individuals opens the possibility to explore cellular crosstalk and to further refine data on cell-cell interactions in the development of CD.
Project description:In this project we profiled small intestinal epithelium, lamina propria immune cells as well as intraepithelial immune cells from 5-weeks old WT mice derived from Jackson laboratories and littermate colonized with segmented filamentous bacteria (SFB) 2 weeks prior to analysis, using 10x droplet-based single-cell RNA sequencing.
Project description:Mouse intestinal innate immune cells have been identified as inducing Th17 cell differentiation. However, few studies have investigated innate immune cells that are involved in CD (Crohn's disiease) pathogenesis in humans. The present study aimed to identify a human intestinal lamina propria cell subset that induces Th17 cells, and to clarify its role in CD pathogenesis. Intestinal mucosa samples were obtained from patients who underwent resection of colorectal cancer or CD. Lamina propria cells (LPCs) were obtained by enzymatic digestion, and were analyzed for expression of HLA-DR, lineage markers (Lin), CD14, and CD163 using flow cytometry. Among HLA-DRhigh Lin- cells, we identified a CD14+ CD163low cell subset that was selectively present in intestinal LPCs. We identified CD14+ CD163low cells as having a potent capacity to induce Th17 cell differentiation in human intestinal lamina propria. The Th17-inducing activity of these cells was enhanced in CD patients. The Cy3-labeled cDNAs were hybridized on Agilent-039494 SurePrint G3 Human GE v2 8x60K Microarray (G4845A) in one color experiments, resulting in four individual microarrays.
Project description:We used RNA sequencing to characterize gene expression of CD4+ CD8α+ double positive (DP), Foxp3+ Treg (TR) and CD4+ single positive (SP) cells in the lamina propria (LP) and intraepithelial compartment (IEL) that had differentiante from the same clonal transnuclear (TN) precursor.
Project description:Mouse intestinal innate immune cells have been identified as inducing Th17 cell differentiation. However, few studies have investigated innate immune cells that are involved in CD (Crohn's disiease) pathogenesis in humans. The present study aimed to identify a human intestinal lamina propria cell subset that induces Th17 cells, and to clarify its role in CD pathogenesis. Intestinal mucosa samples were obtained from patients who underwent resection of colorectal cancer or CD. Lamina propria cells (LPCs) were obtained by enzymatic digestion, and were analyzed for expression of HLA-DR, lineage markers (Lin), CD14, and CD163 using flow cytometry. Among HLA-DRhigh Lin- cells, we identified a CD14+ CD163low cell subset that was selectively present in intestinal LPCs. We identified CD14+ CD163low cells as having a potent capacity to induce Th17 cell differentiation in human intestinal lamina propria. The Th17-inducing activity of these cells was enhanced in CD patients.
Project description:Type 2 immune responses are crucial for protection against helminth infections and for the maintenance of tissue homeostasis, yet the underlying mechanisms of immune activation remain incompletely understood. Here, we study the role of mast cells in type 2 immunity. While the number of lamina propria residing mast cells (termed LPMCs hereinafter) remained stable, intraepithelial mast cells (termed IEMCs hereinafter) markedly expanded during the course of type 2 responses. We uncovered a new type 2 response mechanism depending on the crosstalk between mast cells and epithelial cells, and defined the function of intraepithelial mast cells.
