Evaluation of: Rudd BD, Smit JJ, Flavell RA et al.: Deletion of TLR3 alters the pulmonary immune environment and mucus production during respiratory syncytial virus infection. J. Immunol. 176[3], 1937–1942 [2006]. The detection of a viral pathogen by Toll-like receptors (TLRs) is a crucial component of antiviral immunity. However, there is increasing evidence that specific molecules in the TLR pathways might also play an important role in maintaining a proper immune environment and in the prevention of pathological symptoms of disease. This involvement in the pathogenesis of a disorder has been shown for a number of infectious as well as noninfectious conditions. A recent study investigated the role of TLR3, which recognizes double-stranded RNA, in respiratory syncytial virus (RSV) infection using TLR3-/- mice. Although no differences in viral growth were observed, the results demonstrated significant enhancement in mucus production in the airways of RSV-infected TLR3-/- mice, accompanied by an increase in pulmonary T helper 2-type cytokine expression. These findings indicate that TLRs might be integral parts of an appropriate immune environment in addition to their known function in pathogen recognition and subsequent cytokine production.
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