Project description:Group 3 innate lymphoid cells (ILC3s) are abundant in the developing or healthy intestine to critically support tissue homeostasis in response to microbial cues and other environmental signals. However, during gastrointestinal disease including infections, colorectal cancer, or inflammatory bowel disease (IBD), intestinal ILC3 numbers are dramatically reduced and the remaining ILC3s become dysfunctional which fuels disease and barrier breakdown. To define the underlying transcriptomic changes, we employed RNA sequencing of ILC3s from IBD patients. This may help to gain a deeper understanding of the mechanisms driving these alterations and ultimately lead to novel preventive, diagnostic, or therapeutic opportunities in IBD.
Project description:Here we report metagenomic sequencing data in gut microbiota of autism spectrum disorders (ASD) compared with healthy volunteers (30 for ASD children and 30 for healthy controls, respectively). The genes changed in autistic subjects involved 1,312,364 analytes that compare to 1,335,835 analytes in healthy controls. The number of taxa in autistic subjects were significantly increased as compared to the healthy controls based on the phylum and genus level (P = 0.001). However, the number of species were significantly decreased in autistic subjects (P = 0.001).
Project description:We obtained transcriptome profiling (SAGE-seq) of immune cells purified from LPMC of IBD and non-IBD patients by using next generation sequencing.
Project description:The IBD-Character cohort (Edinburgh, Oslo, Örebro, Linköping, Zaragoza, Maastricht) included patients with inflammatory bowel diseases (IBD: Crohn's disease, ulcerative colitis) recruited at diagnosis and non-IBD controls. Paired-end RNA sequencing was used for whole blood expression profiling. Raw and normalized counts tables are provided.
Project description:We generated genome-wide chromatin-state maps of immune cells purified from LPMC of IBD and non-IBD patients by using next generation sequencing.
Project description:Deficiency in the X-linked inhibitor of apoptosis protein (XIAP) is the cause for the X-linked lymphoproliferative syndrome 2 (XLP2). About one third of all patients suffers from severe and therapy refractory inflammatory bowel disease (IBD), but the exact pathogenesis remains undefined. We examined the differences in gene expression of pediatric XLP2 patients with IBD to healthy controls and pediatric IBD patients.