{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T18:28:22Z","timestamp":1791138502304,"version":"4.1.0"},"reference-count":18,"publisher":"Oxford University Press (OUP)","issue":"10","license":[{"start":{"date-parts":[[2008,11,1]],"date-time":"2008-11-01T00:00:00Z","timestamp":1225497600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2008,11,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>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 wild-type 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-\u03b3, 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.<\/jats:p>","DOI":"10.4049\/jimmunol.181.10.6692","type":"journal-article","created":{"date-parts":[[2014,4,18]],"date-time":"2014-04-18T23:00:36Z","timestamp":1397862036000},"page":"6692-6696","source":"Crossref","is-referenced-by-count":46,"title":["Cutting Edge: Eosinophils Do Not Contribute to Respiratory Syncytial Virus Vaccine-Enhanced Disease"],"prefix":"10.1093","volume":"181","author":[{"given":"Elaine M.","family":"Castilow","sequence":"first","affiliation":[{"name":"Interdisciplinary Graduate Program in Immunology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kevin L.","family":"Legge","sequence":"additional","affiliation":[{"name":"Interdisciplinary Graduate Program in Immunology"},{"name":"Department of Pathology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Steven M.","family":"Varga","sequence":"additional","affiliation":[{"name":"Interdisciplinary Graduate Program in Immunology"},{"name":"Department of Microbiology, University of Iowa , Iowa City, IA 52242"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2008,11,15]]},"reference":[{"key":"2025032608472673400_R1","first-page":"402","article-title":"From the National Institute of Allergy and Infectious Diseases and the World Health Organization. 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Immunol.","year":"2002"},{"key":"2025032608472673400_R15","first-page":"715","article-title":"Novel p19 protein engages IL-12p40 to form a cytokine, IL-23, with biological activities similar as well as distinct from IL-12","volume-title":"Immunity","year":"2000"},{"key":"2025032608472673400_R16","first-page":"827","article-title":"Identification and purification of natural killer cell stimulatory factor (NKSF), a cytokine with multiple biologic effects on human lymphocytes","volume-title":"J. Exp. Med.","year":"1989"},{"key":"2025032608472673400_R17","first-page":"2063","article-title":"Critical role for STAT4 activation by type 1 interferons in the interferon-\u03b3 response to viral infection","volume-title":"Science","year":"2002"},{"key":"2025032608472673400_R18","first-page":"9790","article-title":"Differential type I interferon induction by respiratory syncytial virus and influenza a virus in vivo","volume-title":"J. 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