Th2 cytokines down-regulate TLR expression and function in human intestinal epithelial cells. Gamma interferon augments the intracellular pathway for lipopolysaccharide (LPS) recognition in human intestinal epithelial cells through coordinated up-regulation of LPS uptake and expression of the intracellular Toll-like receptor 4–MD-2 complex. PU.1 and interferon consensus sequence-binding protein regulate the myeloid expression of the human Toll-like receptor 4 gene. Expression of Toll-like receptor 9 and response to bacterial CpG oligodeoxynucleotides in human intestinal epithelium. Pedersen, G., Andresen, L., Matthiessen, M. TLR4 and MD-2 expression is regulated by immune-mediated signals in human intestinal epithelial cells. Regulation of TLR4-associated MD-2 in intestinal epithelial cells: a comprehensive analysis. Mechanisms of cross hyporesponsiveness to Toll-like receptor bacterial ligands in intestinal epithelial cells. Decreased expression of Toll-like receptor-4 and MD-2 correlates with intestinal epithelial cell protection against dysregulated proinflammatory gene expression in response to bacterial lipopolysaccharide. Differential alteration in intestinal epithelial cell expression of Toll-like receptor 3 (TLR3) and TLR4 in inflammatory bowel disease. Innate and adaptive immunity cooperate flexibly to maintain host-microbiota mutualism. TLR signaling mediated by MyD88 is required for a protective innate immune response by neutrophils to Citrobacter rodentium. Toll-like receptor 4 contributes to colitis development but not to host defense during Citrobacter rodentium infection in mice. CX3CR1-mediated dendritic cell access to the intestinal lumen and bacterial clearance. Dendritic cells express tight junction proteins and penetrate gut epithelial monolayers to sample bacteria. Human CD8 + intraepithelial lymphocytes: a unique model to study the regulation of effector cytotoxic T lymphocytes in tissue. The gastrointestinal tract stem cell niche. Manipulating TLR signalling may have a beneficial effect in this setting. TLR signalling promotes the development of APC-dependent colorectal cancers and inflammation-associated colorectal cancers. TLR signalling by IECs leads to the production of cytokines such as a proliferation-inducing ligand (APRIL), which induce class switching to IgA2, a protease-resistant, T cell-independent isotype of IgA. Secretory IgA produced by lamina propria B cells protects against invasion of both commensal organisms and pathogens. The absence of these lectins allows dissemination of intestinal pathogens. MYD88 signalling by Paneth cells is required for the expression of regenerating islet-derived protein 3γ (REG3γ), REG3β, CRP-ductin and resistin-like molecule-β (RELMβ). Paneth cells are specialized epithelial cells located at the base of the small intestinal crypts that produce antimicrobial proteins and lectins. TLRs regulate stem cell proliferation during injury by directing the recruitment of COX2-expressing mesenchymal stromal cells and macrophages, which produce trophic factors including PGE 2 that stimulate stem cell proliferation. Following intestinal injury, TLR4 signalling through myeloid differentiation primary-response protein 88 (MYD88) results in the induction of cyclooxygenase 2 (COX2) expression and the production of prostaglandin E 2 (PGE 2) and amphiregulin, which is an epidermal growth factor family member. TLRs are also expressed by specific types of IEC within the crypt to villus axis, such as enteroendocrine cells, which respond to TLR activation by secreting somatostatin and cholecystokinin.Īctivation of TLRs in IECs results in proliferation, restitution and protection against apoptosis. Polarization of TLRs to the basolateral membrane of the IECs has been described for TLR4, TLR5 and TLR9 and decreases activation in response to luminal commensal bacteria. IECs express several Toll-like receptors (TLRs) including TLR1, TLR2, TLR4, TLR5 and TLR9. A single layer of intestinal epithelial cells (IECs) provides a physical barrier that separates trillions of commensal bacteria in the intestinal lumen from the underlying lamina propria and deeper intestinal layers.
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