Cited by 76Asthma and respiratory diseasesImmune Response and InflammationAllergic Rhinitis and Sensitization

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

Iwamura, Chiaki, Nakayama, Toshinori·2008·Current Allergy and Asthma Reports

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.

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Crossref · 10.1007/s11882-008-0003-0

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  • Infection of human airway epithelial cells with respiratory viruses induces rapid cytokine and chemokine gene expression through activation of proinflammatory transcription factors including NF-kB, AP-1, and STAT1/2.

    “Infection of human airway epithelial cells with respiratory viruses induces rapid cytokine and chemokine gene expression through activation of several proinflammatory transcription factors. These include NF-κB, AP-1, and STAT1/2 (123, 181).”

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Authors
Iwamura, C., & Nakayama, T.
Affiliations
Chiba University (JP)
Corresponding author
Nakayama, Toshinori
Venue
Current Allergy and Asthma Reports
Published
2008-01
Volume
8
Issue
1
Pages
7-13
ISSN
  • 1529-7322 (ISSN-L)
  • 1534-6315
OpenAlex
W2002436848
Cited by
76
References
56
Citations by year
2024: 2 · 2023: 1 · 2022: 4 · 2021: 6 · 2019: 4 · 2018: 2 · 2016: 2 · 2015: 9 · 2014: 5 · 2013: 3 · 2012: 7
FWCI
1.12
Type
journal article
Language
en
Open access
closed
Locations
  • Current Allergy and Asthma Reports (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Physiology › Asthma and respiratory diseases
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
  • Health Sciences › Medicine › Immunology and Allergy › Allergic Rhinitis and Sensitization
Keywords
Toll-like receptors, allergic airway inflammation, asthma, innate immunity, TLR9, Th1/Th2 balance, Th17 cells, mast cells, eosinophils, dendritic cells, airway epithelial cells, IL-5, T cell activation, cytokine production
MeSH terms
Asthma, Dendritic Cells, Eosinophils, Humans, Hypersensitivity, Inflammation, Lymphocyte Activation, Mast Cells, Respiratory System, Signal Transduction, Cytokines, Th1 Cells, Th2 Cells, Toll-Like Receptors

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