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Tollip regulates proinflammatory responses to interleukin-1 and lipopolysaccharide.

Abstract : 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.
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https://www.hal.inserm.fr/inserm-00000043
Contributor : Jean-Claude Sirard <>
Submitted on : Wednesday, December 13, 2006 - 5:07:31 PM
Last modification on : Monday, August 26, 2019 - 12:02:03 PM
Long-term archiving on: : Saturday, April 3, 2010 - 10:57:40 PM

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Arnaud Didierlaurent, Brian Brissoni, Dominique Velin, Natalia Aebi, Aubry Tardivel, et al.. Tollip regulates proinflammatory responses to interleukin-1 and lipopolysaccharide.. Molecular and Cellular Biology, American Society for Microbiology, 2006, 26, pp.735-42. ⟨10.1128/MCB.26.3.735-742.2006⟩. ⟨inserm-00000043⟩

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