Tollip regulates proinflammatory responses to interleukin-1 and lipopolysaccharide. - Archive ouverte HAL Access content directly
Journal Articles Molecular and Cellular Biology Year : 2006

Tollip regulates proinflammatory responses to interleukin-1 and lipopolysaccharide.

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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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Dates and versions

inserm-00000043 , version 1 (13-12-2006)

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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, 2006, 26, pp.735-42. ⟨10.1128/MCB.26.3.735-742.2006⟩. ⟨inserm-00000043⟩
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