In Peli1−/− mice, TLR3 activation in the lung by synthetic agonists, or by infection with rhinovirus or influenza, is characterized by an increased inflammatory response with excess induction of pro-inflammatory cytokines including IL-6 and TNFα, increased capillary leak, and a modulation of the inflammatory immune response seen as an early increase in neutrophils and innate B cells in the airway and a later increase in T-cell populations in the airway and lung. The gene discussed is PELI1; the disease is infection.