Respiratory Syncytial Virus Protects Against the Subsequent Development of Ovalbumin-Induced Allergic Responses by Inhibiting Th2-Type γδ T Cells

Respiratory syncytial virus (RSV) infection has been hypothesized to be a risk factor for the development of allergy and asthma, but epidemiologic studies in humans still remain inconclusive. The association between RSV infection and allergic diseases may be dependent on an atopic background and previous history of RSV infection. It has been reported that RSV infection before sensitization to an allergen decreased the production of Th2-like cytokines in the lung and the levels of allergen-specific Th2-type antibodies in the serum. However, the underlying mechanisms are largely unknown. In the present study, the role of pulmonary ?d T cells in RSV-affected, allergen-induced airway inflammation was investigated. BALB/c mice were sensitized to or challenged with ovalbumin (OVA) and infected with RSV either before or after the sensitization period. It became clear that sensitization and challenge of mice with OVA induced a large influx of ?d T cells to the lungs. However, prior RSV infection inhibited the infiltration of ?d T cells as well as activated ?d T cells, characterized by expression of CD40L or CD69 molecular in the cell surface. Moreover, prior RSV infection elevated the type 1 cytokine gene expression but suppressed type 2 cytokine expression in the lung ?d T cells. Adoptive transfer of ?d T cells from OVA-sensitized and challenged mice increased airway inflammation, suggesting that ?d T cells may play a proinflammatory role in allergic responses. These results described here support the idea of an unknown ?d T cell-dependent mechanism in the regulation of RSV-affected, allergen-induced allergic airway responses. J. Med. Virol. 85:149156, 2012. (c) 2012 Wiley Periodicals, Inc.