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Tollip regulates proinflammatory responses to interleukin-1 and lipopolysaccharide.

http://www.ncbi.nlm.nih.gov/pubmed/16428431

Activation of interleukin-1 (IL-1) receptor (IL-1R), Toll-like receptor 2 (TLR2), and TLR4 triggers NF-kappaB and mitogen-activated protein kinase (MAPK)-dependent signaling, thereby initiating immune responses. Tollip has been implicated as a negative regulator of NF-kappaB signaling triggered by these receptors in in vitro studies. Here, deficient mice were used to determine the physiological contribution of Tollip to immunity. NF-kappaB, as well as MAPK, signaling appeared normal in Tollip-deficient cells stimulated with IL-1beta or the TLR4 ligand lipopolysaccharide (LPS). Similarly, IL-1beta- and TLR-driven activation of dendritic cells and lymphocytes was indistinguishable from wild-type cells. In contrast, the production of the proinflammatory cytokines, IL-6 and tumor necrosis factor alpha was significantly reduced after IL-1beta and LPS treatment at low doses but not at lethal doses of LPS. Tollip therefore controls the magnitude of inflammatory cytokine production in response to IL-1beta and LPS.

Pubmed ID: 16428431 RIS Download

Mesh terms: Animals | Dendritic Cells | Down-Regulation | Interleukin-1 | Interleukin-1 Receptor-Associated Kinases | Interleukin-6 | Intracellular Signaling Peptides and Proteins | Lipopolysaccharides | Lymphocyte Activation | Lymphocytes | Mice | Mice, Mutant Strains | Mitogen-Activated Protein Kinase Kinases | NF-kappa B | Protein-Serine-Threonine Kinases | Toll-Like Receptor 2 | Toll-Like Receptor 4 | Tumor Necrosis Factor-alpha

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