Abstract
Asthma is a chronic airway inflammatory disease that is influenced by the interplay between genetic factors and exposure to environmental allergens, microbes, or microbial products where toll-like receptors (TLRs) play a pivotal role. TLRs recognize a wide range of microbial or endogenous molecules as well as airborne environmental allergens and act as adjuvants that influence positively or negatively allergic sensitization. TLRs are qualitatively and differentially expressed on hematopoietic and non-hematopoietic stromal or structural airway cells that when activated by TLRs agonists exert an immune-modulatory role in asthma development. Therefore, understanding mechanisms and pathways by which TLRs orchestrate asthma outcomes may offer new strategies to control the disease. Here, we aim to review and critically discuss the role of TLRs in human asthma and murine models of allergic airway inflammation, highlighting the complexity of TLRs function in development, exacerbation, or control of airway allergic inflammation.
Highlights
Reviewed by: David Dombrowicz, Institut National de la Santé et de la Recherche Médicale (INSERM), France Ryutaro Fukui, The University of Tokyo, Japan
toll-like receptors (TLRs) are type I transmembrane receptors distinguished by their ligand specificity found on the plasma membrane [TLR1, TLR2, toll-like receptor-4 (TLR4), TLR5, and TLR6] or endosomal compartments of cells (TLR3, TLR7, TLR8, and TLR9) [2]
The therapeutic effects of TLR7 agonist have been evaluated by Nencini et al that reported that conjugation of OH-modified adenine, a novel TLR7 ligand, with both Der p 2 (Der p 2-Conj) and OVA (OVA-Conj) diminished Th2-mediated airway inflammation in an IL-10 and IFN-γ-dependent manner [110], the exact mechanisms by which TLR7 agonists forestall asthma development are still elusive
Summary
Except TLR3 that signals through TRIF, recruit MyD88 adaptor molecule while TLR4 activates both the MyD88-dependant and the endosomal TRIF-dependent pathways. Stimulation of MyD88 pathway by endosomal TLRs (TLR7, TLR8, and TLR9) results in the production of inflammatory cytokines via NF-κB and type I IFNs via IRFs
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