Differentiated control or IBD-derived monolayers were examined for establishment of transepithelial electrical resistance (TEER), loss of barrier integrity in response to a cocktail of interferon (IFN)-γ and tumor necrosis factor (TNF)-α, and prevention of cytokine-induced barrier disruption by the JAK inhibitor, tofacitinib. Cell-type composition was determined by deconvolution of cell-associated gene signatures and histological features. Biological or technical replicates were examined for transcriptional responses under conditions of expansion or differentiation. Patient-derived organoids or monolayers were generated from control or IBD patient–derived colon or ileum and were molecularly or functionally profiled. We profiled molecular and cellular features across a range of intestinal organoid models and examined differentiation and establishment of a functional epithelial barrier. Patient-derived organoid (PDO) models offer potential to transform drug discovery for inflammatory bowel disease (IBD) but are limited by inconsistencies with differentiation and functional characterization.
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