In addition to its role in (myco)bacterial infections, CD14 may also play a role in the pulmonary host response against respiratory syncytial virus (RSV), the most common cause of lower respiratory tract disease in infants and young children worldwide, and infl uenza A virus, a cause of pneumonia in very young children, the elderly and immunocompromised patients. Th e envelop F glycoprotein from RSV and certain infl uenza A virus components activate macrophages in a CD14-dependent manner [14, 20] . Experiments with wild-type and TLR4mutant mice infected intranasally with RSV showed that viral clearance was reduced in the absence of functional TLR4 [14] , due to impaired natural killer (NK) cell migration and function and impaired cytokine secretion. Recently, it was found that TLR2 and TLR6 are also involved in recognition of RSV [49] . Whether CD14 contributes to these TLR-mediated immune responses against RSV remains to be determined. Using CD14defi cient mice, we demonstrated that CD14 played a minimal role in infl uenza A virus-induced pneumonia [50] . During the entire course of disease, viral loads were slightly reduced in CD14-defi cient mice, but this did not result from improved lymphocyte recruitment or lympho cyte activation, or consistent changes in pulmonary cytokines [50] . Th us, despite the fact that infl uenza A expresses ligands that require CD14 for immune cell activation [20] , CD14 seems redundant in the host defense response against infl uenza A virus.