Get 20M+ Full-Text Papers For Less Than $1.50/day. Start a 14-Day Trial for You or Your Team.

Learn More →

Toll-like receptors in the respiratory system: Their roles in inflammation

Toll-like receptors in the respiratory system: Their roles in inflammation Allergic airway inflammation develops in the context of innate immune cells that express Toll-like receptors (TLRs). TLRs recognize microbial components and evoke diverse responses in immune and other respiratory cells through distinct signaling pathways. Bacterial and viral infection in the airway modulates the extent of allergic inflammation. TLR stimulation controls T helper (Th) 1, Th2, and Th17 cell differentiation, cytokine production in mast cells, and activation of eosinophils via direct and indirect pathways. TLR signals in dendritic cells increase expression of major histocompatibility complex proteins and T-cell coreceptors, resulting in greater T-cell activation with Th1 bias. TLR signals in mast cells increase their release of IL-5, and TLR signals in airway epithelial cells enhance airway generation of proallergic cytokines. Although these responses play an important protective role in infection, they may exacerbate allergic inflammation. Under some conditions, TLR stimulation, especially via TLR9, reduces Th2-dependent allergic inflammation through induction of Th1 responses. Therefore, understanding the regulatory role of TLRs in the pathogenesis of allergic airway inflammation may shed light on improving inflammation control in asthmatic patients. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Current Allergy and Asthma Reports Springer Journals

Toll-like receptors in the respiratory system: Their roles in inflammation

Loading next page...
 
/lp/springer-journal/toll-like-receptors-in-the-respiratory-system-their-roles-in-7Ps95gO5tv

References (58)

Publisher
Springer Journals
Copyright
Copyright © 2008 by Springer Science+Business Media, LLC
Subject
Medicine & Public Health; Otorhinolaryngology; Pneumology/Respiratory System; Allergology
ISSN
1529-7322
eISSN
1534-6315
DOI
10.1007/s11882-008-0003-0
Publisher site
See Article on Publisher Site

Abstract

Allergic airway inflammation develops in the context of innate immune cells that express Toll-like receptors (TLRs). TLRs recognize microbial components and evoke diverse responses in immune and other respiratory cells through distinct signaling pathways. Bacterial and viral infection in the airway modulates the extent of allergic inflammation. TLR stimulation controls T helper (Th) 1, Th2, and Th17 cell differentiation, cytokine production in mast cells, and activation of eosinophils via direct and indirect pathways. TLR signals in dendritic cells increase expression of major histocompatibility complex proteins and T-cell coreceptors, resulting in greater T-cell activation with Th1 bias. TLR signals in mast cells increase their release of IL-5, and TLR signals in airway epithelial cells enhance airway generation of proallergic cytokines. Although these responses play an important protective role in infection, they may exacerbate allergic inflammation. Under some conditions, TLR stimulation, especially via TLR9, reduces Th2-dependent allergic inflammation through induction of Th1 responses. Therefore, understanding the regulatory role of TLRs in the pathogenesis of allergic airway inflammation may shed light on improving inflammation control in asthmatic patients.

Journal

Current Allergy and Asthma ReportsSpringer Journals

Published: Jan 30, 2008

There are no references for this article.