title: The active contribution of Toll-like receptors to allergic airway inflammation.
abstract: 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.
authors.affiliation: Laboratory of Molecular Immunoregulation, Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute at Frederick, Frederick, MD 21702, United States.
authors.forename: Keqiang
authors.initials: K
authors.lastname: Chen
authors.forename: Yi
authors.initials: Y
authors.lastname: Xiang
authors.forename: Xiaohong
authors.initials: X
authors.lastname: Yao
authors.forename: Ying
authors.initials: Y
authors.lastname: Liu
authors.forename: Wanghua
authors.initials: W
authors.lastname: Gong
authors.forename: Teizo
authors.initials: T
authors.lastname: Yoshimura
authors.forename: Ji Ming
authors.initials: JM
authors.lastname: Wang
mesh_terms: D000818:Animals; D017951:Antigen Presentation; D001249:Asthma / Q000188:drug therapy / Q000276:immunology*; D002454:Cell Differentiation; D003713:Dendritic Cells / Q000276:immunology; D004804:Eosinophils / Q000276:immunology*; D006801:Humans; D015848:Interleukin-5 / Q000276:immunology; D008407:Mast Cells / Q000276:immunology*; D058990:Molecular Targeted Therapy; D020545:Respiratory Mucosa / Q000276:immunology; D015398:Signal Transduction / Q000276:immunology; D058408:Th1-Th2 Balance; D018418:Th2 Cells / Q000276:immunology*; D051193:Toll-Like Receptors / Q000276:immunology*
chemical_list: D015848:Interleukin-5; D051193:Toll-Like Receptors