Asthma is one of the common respiratory diseases characterized by persistent or non-resolving allergen-driven inflammation. Toll-like receptors (TLRs), a member of pattern recognition receptors (PRRs), have been suggested to contribute to the initiation and perpetuation of airway inflammation, by virtue of their ability as the host's first line defense to recognize invading pathogens and aeroallergens (1). Within the TLRs family, TLR2 is regarded as the major one responsible for the sustaining airway inflammation and thus be most relevant to the onset of asthma (2–4). However, despite more and more advances in our understanding of the role of TLR2 in allergic asthma, the mechanism underlying TLR2 regulation in allergic airway inflammation is still elusive.