In humans and mice, sensitisation to respiratory syncytial virus (RSV) antigens can result in severe inflammatory lung disease during subsequent infection with the virus. Although specific antiviral T cells are thought to be responsible for this augmentation of disease, the precise role of different functional subsets is unknown. BALB/c mice sensitised to the major surface glycoprotein (G) of RSV expressed by recombinant vaccinia virus develop Th2-driven lung eosinophilia after intranasal challenge with the virus. Mice treated with IL-12 at various times during vaccination and challenge, had reduced vaccine-induced lung eosinophilia but increased total pulmonary lymphoid cell infiltration. Intracellular cytokine analysis showed that interferon-gamma production during challenge was increased and IL-4 and IL-5 reduced by IL-12 treatment. Though IL-12 treatment reduced lung eosinophilia, illness (as assessed by weight loss) was not eliminated and sometimes increased. Reversing Th2-associated pathology with IL-12 does not necessarily benefit the host.