Mucosa of the nose and nasopharynx is the first site of contact with inhaled antigens and primary target of infection by RSV. Processing and presentation of viral antigenic peptides by respiratory epithelial cells of the upper airways may determine the nature of local and systemic immune responses to RSV, ultimately leading to protection or to enhanced disease. In this study, we have characterized the expression of Class II MHC antigens, the accessory ligands ICAM-1 and VCAM-1 and of polymeric Ig receptor (pIg-R) by primary cultures of human nose- and adenoid-derived epithelial cells. Confluent monolayers of epithelial cells were infected with RSV (strain A2) at a multiplicity of infection of 1 or were exposed to rIFN-γ (100 U/ml) for 48 hr and cell surface expression of these molecules was determined by cell-based ELISA method. Low levels of class II MHC were expressed on unstimulated epithelial cells. RSV infection of IFN-γ stimulation induced 2 and 4-fold increase respectively in class II MHC expression. ICAM-1 was highly expressed on untreated nasal epithelial cells and was only slightly increased by RSV infection (13%) or IFN-γ stimulation (36%). On the other hand, VCAM-1, undetectable on uninfected cells, was induced in about half of the cultures, by RSV infection or by treatment with TNF-α (100 U/ml), as confirmed also by the expression of specific mRNA. PIg-R was constitutively expressed on both nasal- and adenoid-derived epithelial cells and its expression was increased by RSV infection (13%) and IFN-γ stimulation (40%). In conclusion, these data show that infection or exposure to inflammatory cytokines of primary human upper respiratory epithelial cells induces/enhances the expression of class II MHC molecules, accessory ligands and pIg-R. These molecules may play an essential role in cell-mediated immune response and in the local secretory immunity to RSV.