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- W2327286908 abstract "BackgroundSignaling via B7 family co-stimulators is crucial in the antigen presenting cells (APCs)-mediated regulation of T cell activity under mucosal tolerance and in its disregulation involved in inflammatory bowel disease (IBD). The expression by APCs of Th1 supressing co-stimulator B7-H1 and Th2 promoting co-stimulator B7-H2 (ICOSL) is critical in suppression of activated Th1 cell responses during mucosal homeostasis. Human CD90+ stromal cells, a.k.a. myofibroblasts/fibroblasts (CMFs) express B7-H2 and are major B7-H1 expressing cells in the normal colonic mucosa. Thus, they may contribute to the tuning of the Th1/Th2 balance. MyD88-dependent TLR stimulation by microbial ligands is important in the modulation of B7 molecule expression on professional APCs. However, little is known regarding how the expression of B7- costimulators on CMFs is influenced by TLR ligands reaching the mucosal lamina propria during mucosal disruption or wound healing or during IBD where the epithelial barrier is breached. Our initial data demonstrate that human normal CMF cultures may upregulate the B7-H1 expression via the MyD88 adaptor involving TLR4 and 5 pathways. Herein, we extend this study and determine the role of MyD88 involving TLRs pathways in the regulation of B7-H1 and B7-H2 expression in murine CMFs in vitro and in vivo." @default.
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- W2327286908 date "2011-12-01" @default.
- W2327286908 modified "2023-09-23" @default.
- W2327286908 title "MyD88-dependent TLR pathways regulate B7 co-stimulator expression by stromal cells in the colonic mucosa" @default.
- W2327286908 doi "https://doi.org/10.1097/00054725-201112002-00219" @default.
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