Journal
JOURNAL OF IMMUNOLOGY
Volume 181, Issue 10, Pages 6692-6696Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.181.10.6692
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Funding
- American Heart Association Midwest Affiliate Predoctoral Fellowship [0815540G]
- Department of Pathology Start-Up Funds
- National Institutes of Health [AI 063520]
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Respiratory syncytial virus (RSV) infection of BALB/c mice previously immunized with a recombinant vaccinia virus (vacv) expressing the attachment (G) protein of RSV (vacvG) results in pulmonary eosinophilia, which mimics the response of formalin-inactivated RSV-vaccinated children, as well as increased weight loss, clinical illness, and enhanced pause (Penh). We show that RSV infection of eosinophil-deficient mice previously immunized with vacvG results in the development of increased weight loss, clinical illness, and Penh similar to that in wildtype controls. These measures of RSV vaccine-enhanced disease are dependent upon STAT4. Interestingly, neither IL-12 nor IL-23, the two most common STAT4-activating cytokines, proved necessary for the development of disease. We demonstrate that IFN-gamma, which is produced following STAT4 activation, contributes to clinical illness and increased Penh, but not weight loss. Our results have important implications for future RSV vaccine design, suggesting that enhancing a Th1 response may exacerbate disease. The Journal of Immunology, 2008, 181: 6692-6696.
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