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First published online 20 November 2002
doi: 10.1242/jcs.00212
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Research Article |
1 Lymphocyte development, URA-1961 of the National Center for Scientific
Research, Pasteur Institute, Paris, France
2 Pathogénie Microbienne Moléculaire, Unité INSERM U389,
Institut Pasteur, Paris, France
3 Department of Host Defense, Research Institute for Microbial Diseases, Osaka
University, Osaka, Japan
4 Défense Innée et Inflammation, Unité associée
IP/Inserm Z485, Institut Pasteur, Paris, France
5 Endotoxin Group, UMR-8619 of the National Center for Scientific Research,
University of Paris-Sud, Orsay, France
* Author for correspondence (e-mail: richard.chaby{at}bbmpc.u-psud.fr)
Accepted 8 October 2002
Lipopolysaccharide (LPS) derived from enterobacteria elicit in several cell types cellular responses that are restricted in the use of Toll-like receptor 4 (TLR4) as the principal signal-transducing molecule. A tendency to consider enterobacterial LPS as a prototypic LPS led some authors to present this mechanism as a paradigm accounting for all LPSs in all cell types. However, the structural diversity of LPS does not allow such a general statement. By using LPSs from bacteria that do not belong to the Enterobacteriaceae, we show that in bone marrow cells (BMCs) the LPS of Rhizobium species Sin-1 and of three strains of Legionella pneumophila require TLR2 rather than TLR4 to elicit the expression of CD14. In addition, exposure of BMCs from TLR4-deficient (C3H/HeJ) mice to the lipid A fragment of the Bordetella pertussis LPS inhibits their activation by the Legionella lipid A. The data show selective action of different LPSs via different TLRs, and suggest that TLR2 can interact with many lipid A structures, leading to either agonistic or specific antagonistic effects.
Key words: Lipopolysaccharide, Toll-like receptors, Bone marrow, CD14, Innate immunity
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