CD14 is required for influenza A virus-induced cytokine and chemokine production.

Infection of monocytes and macrophages by influenza A virus leads to proinflammatory and chemotactic cytokine production. The signalling pathways linking innate immune virus recognition to cytokine expression are little understood. Here, we report that blocking of CD14 on human monocytes by specific antibody or use of CD14-deficient murine macrophages abolished influenza A virus-induced cytokine production. Toll-like receptor (TLR) 2 and 4-deficient murine macrophages remained fully responsive. These results suggest that CD14, together with a TLR other than TLR2 or 4, is an essential coreceptor of the influenza A virus sensing recognition system.