The active contribution of Toll-like receptors to allergic airway inflammation

Keqiang Chen, Yi Xiang, Xiaohong Yao, Ying Liu, Wanghua Gong, Teizo Yoshimura, Ji Ming Wang

Research output: Contribution to journalArticlepeer-review

49 Citations (Scopus)


Epithelia lining the respiratory tract represent a major portal of entry for microorganisms and allergens and are equipped with innate and adaptive immune signaling receptors for host protection. These include Toll-like receptors (TLRs) that recognize microbial components and evoke diverse responses in cells of the respiratory system. TLR stimulation by microorganism-derived molecules activates antigen presenting cells, control T helper (Th) 1, Th2, and Th17 immune cell differentiation, cytokine production by mast cells, and activation of eosinophils. It is clear that TLR are involved in the pathophysiology of allergic airway diseases such as asthma. Dendritic cells (DCs), a kind of antigen presenting cells, which play a key role in the induction of allergic airway inflammation, are privileged targets for pathogen associated molecular patterns (PAMPs). During the allergic responses, engagement of TLRs on DCs determines the Th2 polarization of the T cells. TLR signaling in mast cells increases the release of IL-5, and TLR activation of airway epithelial cells forces the generation of proallergic Th2 type of cytokines. Although these responses aim to protect the host, they may also result in inflammatory tissue damage in the airway. Under certain conditions, stimulation of TLRs, in particular, TLR9, may reduce Th2-dependent allergic inflammation by induction of Th1 responses. Therefore, understanding the complex regulatory roles of TLRs in the pathogenesis of allergic airway inflammation should facilitate the development of preventive and therapeutic measures for asthmatic patients.

Original languageEnglish
Pages (from-to)1391-1398
Number of pages8
JournalInternational Immunopharmacology
Issue number10
Publication statusPublished - Oct 2011
Externally publishedYes


  • Allergic airway inflammation
  • Host response
  • TLRs

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Pharmacology


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