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Clinical Microbiology Reviews, October 2003, p. 637-646, Vol. 16, No. 4
0893-8512/03/$08.00+0     DOI: 10.1128/CMR.16.4.637-646.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Role of Toll-Like Receptors in Pathogen Recognition

S. Janssens and R. Beyaert*

Unit for Molecular Signal Transduction in Inflammation, Department of Molecular Biomedical Research, Ghent University VIB, B-9052 Ghent, Belgium

The innate immune system relies on a vast array of non-clonally expressed pattern recognition receptors for the detection of pathogens. Pattern recognition receptors bind conserved molecular structures shared by large groups of pathogens, termed pathogen-associated molecular patterns. The Toll-like receptors (TLRs) are a recently discovered family of pattern recognition receptors which show homology with the Drosophila Toll protein and the human interleukin-1 receptor family. Engagement of different TLRs can induce overlapping yet distinct patterns of gene expression that contribute to an inflammatory response. The TLR family is characterized by the presence of leucine-rich repeats and a Toll/interleukin-1 receptor-like domain, which mediate ligand binding and interaction with intracellular signaling proteins, respectively. Most TLR ligands identified so far are conserved microbial products which signal the presence of an infection, but evidence for some endogenous ligands that might signal other danger conditions has also been obtained. Molecular mechanisms for pathogen-associated molecular pattern recognition still remain elusive but seem to be more complicated than initially anticipated. In most cases, direct binding of microbial ligands to TLRs still has to be demonstrated. Moreover, Drosophila TLRs bind endogenous ligands, generated through a proteolytic cascade in response to an infection. In the case of endotoxin, recognition involves a complex of TLR4 and a number of other proteins. Moreover, TLR heterodimerization further extends the spectrum of ligands and modulates the response towards specific ligands. The fact that TLR expression is regulated in both a cell type- and stimulus-dependent fashion further contributes to the complexity.

* Corresponding author. Mailing address: Department of Molecular Biomedical Research, Unit for Molecular Signal Transduction in Inflammation, Ghent University - VIB, Technologiepark 927, B-9052 Ghent, Belgium Phone: 32 93313770. Fax: 32 93313609. E-mail: rudi.beyaert{at}dmbr.Ugent.be.

Clinical Microbiology Reviews, October 2003, p. 637-646, Vol. 16, No. 4
0893-8512/03/$08.00+0     DOI: 10.1128/CMR.16.4.637-646.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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