Targeting TLR/IL-1R Signalling in Human Diseases

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 h...

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Main Authors: Maria Loiarro (Author), Vito Ruggiero (Author), Claudio Sette (Author)
Format: Book
Published: Hindawi Limited, 2010-01-01T00:00:00Z.
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100 1 0 |a Maria Loiarro  |e author 
700 1 0 |a Vito Ruggiero  |e author 
700 1 0 |a Claudio Sette  |e author 
245 0 0 |a Targeting TLR/IL-1R Signalling in Human Diseases 
260 |b Hindawi Limited,   |c 2010-01-01T00:00:00Z. 
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500 |a 10.1155/2010/674363 
520 |a 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. 
546 |a EN 
690 |a Pathology 
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786 0 |n Mediators of Inflammation, Vol 2010 (2010) 
787 0 |n http://dx.doi.org/10.1155/2010/674363 
787 0 |n https://doaj.org/toc/0962-9351 
787 0 |n https://doaj.org/toc/1466-1861 
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