BALB/c mice vaccinated with vaccinia virus expressing the major surface glycoprotein G of respiratory syncytial virus (RSV) develop lung eosinophilia during RSV challenge. The G protein is remarkable in that it induces CD4⁺, but no CD8⁺ T cells in this mouse strain. Studies using passive T cell transfers show that co‐injection of CD8⁺ T cells greatly reduces the Th2‐driven lung eosinophilia caused by G‐specific CD4⁺ T cells. By contrast, vaccination with the fusion protein (F) induces both CD8⁺ and CD4⁺ T cells, but not lung eosinophilia during RSV infection. These observations suggest that CD8⁺ T cells play a crucial role in preventing Th2‐driven pathology. We therefore depleted mice with anti‐CD8 antibodies in vivo. This treatment allowed lung eosinophilia to develop in F‐primed mice. Depletion of interferon (IFN)‐γ had a similar effect, suggesting that secretion of this cytokine is the mechanism by which CD8⁺ T cells exert their effect. To test whether similar effects occurred in other strains of mice, RSV‐infected C57BL/6 mice (which do not develop eosinophilia after sensitization to G) were treated with anti‐IFN‐γ. Again, these mice developed eosinophilia. In this strain, genetic deletion of CD8‐α, β2‐microglobulin or genes coding for the transporter associated with antigen presentation (which in each case eliminates CD8⁺ T cells) caused lung eosinophilia during RSV infection. These studies show the critical roles that CD8⁺ T cells and IFN‐γ production play in regulating Th2‐driven eosinophilia and provide a unifying explanation for previous studies of lung eosinophilia. We propose that vaccines designed to enhance CD8⁺ T cell recognition might avoid disease caused by CD4⁺ Th2 cells.