LAUSR

Recent advances indicate that there is crosstalk between allergic disorders and nucleic acid sensing. Triggers that activate inflammatory mechanisms via nucleic acid sensors affect both allergic phenotypes and anti-viral responses, depending on the timing and the order of exposure. Viral respiratory infections, such as those caused by the rhinovirus, influenza, and respiratory syncytial virus, are the most frequent cause of significant asthma exacerbations through effects mediated predominantly by TLR3. However, agonists of other nucleic acid sensors, such as TLR7/8 and TLR9 agonists, may inhibit allergic inflammation and reduce clinical manifestations of disease. The allergic state can predispose the immune system to both exaggerated responses to viral infections or protection from anti-viral inflammatory responses. TH2 cytokines appear to alter the epithelium, leading to defective viral clearance or exaggerated responses to viral infections. However, a TH2 skewed allergic response may be protective against a TH1-dependent inflammatory anti-viral response. This review briefly introduces the receptors involved in nucleic acid sensing, addresses mechanisms by which nucleic acid sensing and allergic responses can counteract one another, and discusses the strategies in experimental settings, both in animal and human studies, to harness the nucleic acid sensing machinery for the intervention of allergic disorders.