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Molecular and Cellular Biology, February 2006, p. 735-742, Vol. 26, No. 3
0270-7306/06/$08.00+0     doi:10.1128/MCB.26.3.735-742.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Tollip Regulates Proinflammatory Responses to Interleukin-1 and Lipopolysaccharide

Arnaud Didierlaurent ,1,{dagger},{ddagger} Brian Brissoni,1,{dagger} Dominique Velin,2 Natalia Aebi,1 Aubry Tardivel,1 Edgar Käslin,1 Jean Claude Sirard,3 Georgi Angelov,4 Jürg Tschopp,1,{dagger} and Kimberly Burns1*,{dagger}

Department of Biochemistry, University of Lausanne, BIL Biomedical Research Center, Chemin des Boveresses 155, CH-1066 Epalinges, Switzerland,1 Department of Gastroenterology, CHUV, BH 18-521, Rue du Bugnon 46, CH-1011 Lausanne, Switzerland,2 INSERM, E0364, Institut de Biologie-Institut Pasteur de Lille, 1 Rue du Pr Calmette, 59021 Lille, France,3 Ludwig Institute for Cancer Research, Chemin des Boveresses 155, CH-1066 Epalinges, Switzerland4

Received 21 April 2005/ Returned for modification 1 June 2005/ Accepted 25 October 2005

Activation of interleukin-1 (IL-1) receptor (IL-1R), Toll-like receptor 2 (TLR2), and TLR4 triggers NF-{kappa}B and mitogen-activated protein kinase (MAPK)-dependent signaling, thereby initiating immune responses. Tollip has been implicated as a negative regulator of NF-{kappa}B signaling triggered by these receptors in in vitro studies. Here, deficient mice were used to determine the physiological contribution of Tollip to immunity. NF-{kappa}B, as well as MAPK, signaling appeared normal in Tollip-deficient cells stimulated with IL-1ß or the TLR4 ligand lipopolysaccharide (LPS). Similarly, IL-1ß- 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-1ß 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-1ß and LPS.

* Corresponding author. Mailing address: Department of Biochemistry, Ch. des Boveresses 155, CH-1066 Epalinges, Switzerland. Phone: 41 21 692 5738. Fax: 41 21 692 5705. E-mail: KimberlyA.BurnsDiMarco{at}unil.ch.

{dagger} A.D., B.B., J.T., and K.B. contributed equally to this study.

{ddagger} Present address: Kennedy Institute of Rheumatology, Imperial College of London, 1 Aspenlea Rd., London W6 8LH, United Kingdom.

Molecular and Cellular Biology, February 2006, p. 735-742, Vol. 26, No. 3
0270-7306/06/$08.00+0     doi:10.1128/MCB.26.3.735-742.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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