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Mediators of Inflammation
Volume 2010, Article ID 674363, 12 pages
http://dx.doi.org/10.1155/2010/674363
Review Article

Targeting TLR/IL-1R Signalling in Human Diseases

1Department of Public Health and Cell Biology, University of Rome “Tor Vergata”, 00133 Rome, Italy
2Laboratory of Neuroembryology, Fondazione Santa Lucia, Istituto Di Ricovero e Cura a Carattere Scientifico (IRCCS), 00143 Rome, Italy
3Department of Immunology (Bldg. LABIO), R&D Sigma-tau Industrie Farmaceutiche Riunite S.p.A, Via Pontina km 30.400, 00040 Pomezia (RM), Italy

Received 1 December 2009; Revised 16 January 2010; Accepted 17 January 2010

Academic Editor: Natalija Novak

Copyright © 2010 Maria Loiarro et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

The members of Toll-like receptor/Interleukin (IL)-1 receptor (TLR/IL-1R) superfamily play a fundamental role in the immune response. These receptors detect microbial components and trigger complex signalling pathways that result in increased expression of multiple inflammatory genes. On the other hand, an aberrant activation of TLR/IL-1R signalling can promote the onset of inflammatory and autoimmune diseases, raising the interest in the development of therapeutic strategies for the control of their function. In this review, we illustrate the structural and functional features of TLR/IL-1R proteins and discuss some recent advances in the approaches undertaken to develop anti-inflammatory therapeutic drugs. In particular, we will focus on inhibitors, such as decoy peptides and synthetic mimetics, that interfere with protein-protein interactions between signalling molecules of the TLR/IL-1R superfamily. Given their central role in innate and adaptive immune responses, it is foreseen that pharmaceutical modulation of TLR/IL-1R signalling pathways by these drugs might yield clinical benefits in the treatment of inflammatory and autoimmune diseases.