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In this study, we examined the role of Fas\/FasL pathway in inflammatory and antiviral response in lungs using a mousepox model applied to C57BL6\/J, B6. MRL\u2010Faslpr\/J, and B6Smn.C3\u2010Faslgld\/J mice. Ectromelia virus (ECTV) infection of Fas\u2010 and FasL\u2010deficient mice led to increased virus titers in lungs  and decreased migration of IFN\u2010<jats:italic>\u03b3<\/jats:italic> expressing NK cells, CD4+ T cells, CD8+ T cells, and decreased IL\u201015 expression. The lungs of ECTV\u2010infected Fas\u2010 and FasL\u2010deficient mice showed significant inflammation during later phases of infection accompanied by decreased expression of anti\u2010inflammatory IL\u201010 and TGF\u2010<jats:italic>\u03b2<\/jats:italic>1 cytokines and disturbances in CXCL1 and CXCL9 expression.  Experiments in vitro demonstrated that ECTV\u2010infected cultures of epithelial cells, but not macrophages, upregulate Fas and FasL and are susceptible to Fas\u2010induced apoptosis.  Our study demonstrates that Fas\/FasL pathway during ECTV infection of the lungs plays an important role in controlling local inflammatory response and mounting of antiviral response.<\/jats:p>","DOI":"10.1155\/2015\/281613","type":"journal-article","created":{"date-parts":[[2015,3,22]],"date-time":"2015-03-22T21:02:43Z","timestamp":1427058163000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":20,"title":["Fas\/FasL Pathway Participates in Regulation of Antiviral and Inflammatory Response during Mousepox Infection of 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