Targeting TLR/IL-1R signalling in human diseases

Vito Ruggiero, Maria Loiarro, Claudio Sette

Research output: Contribution to journalArticle

55 Citations (Scopus)

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.

Original languageEnglish
Article number674363
JournalMediators of Inflammation
Volume2010
DOIs
Publication statusPublished - 2010

Fingerprint

Interleukin-1 Receptors
Toll-Like Receptors
Autoimmune Diseases
Toll-Like Receptor 1
Pharmaceutical Preparations
Proteins
Adaptive Immunity
Innate Immunity
Anti-Inflammatory Agents
Peptides

ASJC Scopus subject areas

  • Cell Biology
  • Immunology

Cite this

Targeting TLR/IL-1R signalling in human diseases. / Ruggiero, Vito; Loiarro, Maria; Sette, Claudio.

In: Mediators of Inflammation, Vol. 2010, 674363, 2010.

Research output: Contribution to journalArticle

Ruggiero, Vito ; Loiarro, Maria ; Sette, Claudio. / Targeting TLR/IL-1R signalling in human diseases. In: Mediators of Inflammation. 2010 ; Vol. 2010.
@article{5d99606aa04241a7a229c5826bd9c63b,
title = "Targeting TLR/IL-1R signalling in human diseases",
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.",
author = "Vito Ruggiero and Maria Loiarro and Claudio Sette",
year = "2010",
doi = "10.1155/2010/674363",
language = "English",
volume = "2010",
journal = "Mediators of Inflammation",
issn = "0962-9351",
publisher = "Hindawi Publishing Corporation",

}

TY - JOUR

T1 - Targeting TLR/IL-1R signalling in human diseases

AU - Ruggiero, Vito

AU - Loiarro, Maria

AU - Sette, Claudio

PY - 2010

Y1 - 2010

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=77952469125&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=77952469125&partnerID=8YFLogxK

U2 - 10.1155/2010/674363

DO - 10.1155/2010/674363

M3 - Article

C2 - 20396389

AN - SCOPUS:77952469125

VL - 2010

JO - Mediators of Inflammation

JF - Mediators of Inflammation

SN - 0962-9351

M1 - 674363

ER -