Abstract
Toll-like receptors (TLRs) play crucial roles in innate immune responses to viral pathogens, and TLR-mediated virus detection is well established to often induce type I IFN production from lung epithelial cells, the principal target cell of many respiratory viruses. Methods: Primary mouse tracheal epithelial cells (mTECs) were treated with Pam2-ODN (or sham) prior to infection with influenza A or Sendai virus, then protein levels of type I IFN were assessed by ELISA.