{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,17]],"date-time":"2026-09-17T12:34:43Z","timestamp":1789648483128,"version":"4.0.0"},"reference-count":54,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2013,6,18]],"date-time":"2013-06-18T00:00:00Z","timestamp":1371513600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur J Immunol"],"published-print":{"date-parts":[[2013,7]]},"abstract":"<jats:p><jats:styled-content style=\"fixed-case\">J<\/jats:styled-content>apanese encephalitis, caused by infection with the neurotropic flavivirus, <jats:styled-content style=\"fixed-case\">J<\/jats:styled-content>apanese encephalitis virus (<jats:styled-content style=\"fixed-case\">JEV<\/jats:styled-content>), is among the most important viral encephalitides in <jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>sia. While previous studies established an essential role of <jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>b and type I <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content>, it is still unclear if the cell\u2010mediated immune responses, through their direct antiviral effector functions, contribute to protection against the fatal disease. We report here that mice defective in both the granule exocytosis and death receptor pathways of cytotoxicity display increased susceptibility to <jats:styled-content style=\"fixed-case\">JEV<\/jats:styled-content>. The two cell contact\u2010dependent cytotoxic effector mechanisms act redundantly within the <jats:styled-content style=\"fixed-case\">CNS<\/jats:styled-content> to reduce disease severity. We also demonstrate that <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content>\u2010\u03b3 is critical in recovery from primary infection with <jats:styled-content style=\"fixed-case\">JEV<\/jats:styled-content> by a mechanism involving suppression of virus growth in the <jats:styled-content style=\"fixed-case\">CNS<\/jats:styled-content>, and that <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content> cells are the main source of the cytokine that promotes viral clearance from the brain. Finally, we show by in vivo depletion of <jats:styled-content style=\"fixed-case\">NK<\/jats:styled-content> cells that this innate immune cell population is dispensable for control of <jats:styled-content style=\"fixed-case\">JEV<\/jats:styled-content> infection in the periphery and in the <jats:styled-content style=\"fixed-case\">CNS<\/jats:styled-content>. Accordingly, cell contact\u2010dependent cytolytic and <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content>\u2010\u03b3\u2010dependent noncytolytic clearance of virus mediated by <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content> cells trafficking into the <jats:styled-content style=\"fixed-case\">CNS<\/jats:styled-content> help in recovery from lethal infection in a mouse model of <jats:styled-content style=\"fixed-case\">J<\/jats:styled-content>apanese encephalitis.<\/jats:p>","DOI":"10.1002\/eji.201243152","type":"journal-article","created":{"date-parts":[[2013,4,9]],"date-time":"2013-04-09T08:12:56Z","timestamp":1365495176000},"page":"1789-1798","source":"Crossref","is-referenced-by-count":57,"title":["Cytolytic effector pathways and <scp>IFN<\/scp>\u2010\u03b3 help protect against <scp>J<\/scp>apanese 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