{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,3]],"date-time":"2026-07-03T01:09:49Z","timestamp":1783040989387,"version":"3.54.6"},"reference-count":52,"publisher":"National Academy of Sciences","issue":"12","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2001,6,5]]},"abstract":"<jats:p>\n                    We inoculated BALB\/c mice deficient in STAT6 (STAT6\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    ) and their wild-type (wt) littermates (STAT6\n                    <jats:sup>+\/+<\/jats:sup>\n                    ) with the natural mouse pathogen, ectromelia virus (EV). STAT6\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice exhibited increased resistance to generalized infection with EV when compared with STAT6\n                    <jats:sup>+\/+<\/jats:sup>\n                    mice. In the spleens and lymph nodes of STAT6\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice, T helper 1 (Th1) cytokines were induced at earlier time points and at higher levels postinfection when compared with those in STAT6\n                    <jats:sup>+\/+<\/jats:sup>\n                    mice. Elevated levels of NO were evident in plasma and splenocyte cultures of EV-infected STAT6\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice in comparison with STAT6\n                    <jats:sup>+\/+<\/jats:sup>\n                    mice. The induction of high levels of Th1 cytokines in the mutant mice correlated with a strong natural killer cell response. We demonstrate in genetically susceptible BALB\/c mice that the STAT6 locus is critical for progression of EV infection. Furthermore, in the absence of this transcription factor, the immune system defaults toward a protective Th1-like response, conferring pronounced resistance to EV infection and disease progression.\n                  <\/jats:p>","DOI":"10.1073\/pnas.111151098","type":"journal-article","created":{"date-parts":[[2002,7,26]],"date-time":"2002-07-26T10:44:19Z","timestamp":1027680259000},"page":"6812-6817","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":28,"title":["Enhanced resistance in STAT6-deficient mice to infection with ectromelia virus"],"prefix":"10.1073","volume":"98","author":[{"given":"Surendran","family":"Mahalingam","sequence":"first","affiliation":[{"name":"Division of Biochemistry and Molecular Biology, The John Curtin School of Medical Research, Australian National University, Canberra ACT 2601, Australia; Department of Pathology, Division of Faculty of Medicine, Blackburn Building, D06, University of Sydney, Sydney NSW 2006, Australia; Department of Host Defense, Research Institute for Microbial Disease, Osaka University, Suita-shi, Osaka 565-0871, Japan; and Department of Biochemistry, Hyogo College of Medicine, 1-1 Mukogawa-cho, ..."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gunasegaran","family":"Karupiah","sequence":"additional","affiliation":[{"name":"Division of Biochemistry and Molecular Biology, The John Curtin School of Medical Research, Australian National University, Canberra ACT 2601, Australia; Department of Pathology, Division of Faculty of Medicine, Blackburn Building, D06, University of Sydney, Sydney NSW 2006, Australia; Department of Host Defense, Research Institute for Microbial Disease, Osaka University, Suita-shi, Osaka 565-0871, Japan; and Department of Biochemistry, Hyogo College of Medicine, 1-1 Mukogawa-cho, 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