• Chiaki Iwamura and Toshinori Nakayama.
• Department of Immunology (H3), Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan.
• Curr Allergy Asthma Rep. 2008 Mar 1;8(1):7-13.

AbstractAllergic 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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