Monocytes Contribute to IFN-beta Production via the MyD88-Dependent Pathway and Cytotoxic T-Cell Responses against Mucosal Respiratory Syncytial. Virus Infection

Abstract

Respiratory syncytial virus (RSV) is the leading cause of respiratory viral infection in infants and children. However, little is known about the contribution of monocytes to antiviral responses against RSV infection. We identified the IFN-beta production of monocytes using IFN-beta/YFP reporter mice. The kinetic analysis of IFN-beta-producing cells in in vivo RSV-infected lung cells indicated that monocytes are recruited to the inflamed lung during the early phase ofinfection. These cells produced IFN-beta via the myeloid differentiation factor 88-mediated pathway, rather than the TLR7- or mitochondrial antiviral signaling protein-mediated pathway. In addition, monocyte-ablated mice exhibited decreased numbers of IFN-gamma-producing and RSV Ag-specific CD8(+) T cells. Collectively, these data indicate that monocytes play pivotal roles in cytotoxic T-cell responses and act as type HFN producers during RSV infection.