{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,10]],"date-time":"2026-09-10T14:47:20Z","timestamp":1789051640476,"version":"build-2803163510"},"reference-count":35,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2011,4,26]],"date-time":"2011-04-26T00:00:00Z","timestamp":1303776000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100000925","name":"National Health and Medical Research Council","doi-asserted-by":"publisher","award":["461219"],"award-info":[{"award-number":["461219"]}],"id":[{"id":"10.13039\/501100000925","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Immunol Cell Biol"],"published-print":{"date-parts":[[2012,1]]},"abstract":"<jats:p>\n                    The lack of expression of the suppressor of cytokine signalling\u20103 (SOCS3) or inactivation of the negative regulatory capacity of SOCS3 has been well documented in rheumatoid arthritis, viral hepatitis and cancer. The specific qualitative and quantitative consequences of SOCS3 deficiency on interleukin\u20106 (IL\u20106)\u2010mediated pro\u2010 and anti\u2010inflammatory responses remain controversial\n                    <jats:italic>in vitro<\/jats:italic>\n                    and unknown\n                    <jats:italic>in vivo<\/jats:italic>\n                    . Mice with a conditional deletion of SOCS3 in hematopoietic cells develop lethal inflammatory disease during adult life and develop gross histopathological changes during experimental arthritis, typified by elevated IL\u20106 levels. To clarify the nature of the IL\u20106 responses\n                    <jats:italic>in vivo<\/jats:italic>\n                    , we generated mice deficient in SOCS3 (\n                    <jats:italic>SOCS3<\/jats:italic>\n                    <jats:sup>\n                      \u2212\/\u0394\n                      <jats:italic>vav<\/jats:italic>\n                    <\/jats:sup>\n                    ) or both SOCS3 and IL\u20106 (\n                    <jats:italic>IL\u20106<\/jats:italic>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    <jats:italic>\/SOCS3<\/jats:italic>\n                    <jats:sup>\n                      \u2212\/\u0394\n                      <jats:italic>vav<\/jats:italic>\n                    <\/jats:sup>\n                    ), and examined responses in models of acute and chronic inflammation. Acute responses to IL\u20101\u03b2 were lethal to\n                    <jats:italic>SOCS3<\/jats:italic>\n                    <jats:sup>\n                      \u2212\/\u0394\n                      <jats:italic>vav<\/jats:italic>\n                    <\/jats:sup>\n                    mice but not\n                    <jats:italic>IL\u20106<\/jats:italic>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    <jats:italic>\/SOCS3<\/jats:italic>\n                    <jats:sup>\n                      \u2212\/\u0394\n                      <jats:italic>vav<\/jats:italic>\n                    <\/jats:sup>\n                    mice, indicating that IL\u20106 was required for the lethal inflammation induced by IL\u20101\u03b2. Administration of IL\u20101\u03b2 to\n                    <jats:italic>SOCS3<\/jats:italic>\n                    <jats:sup>\n                      \u2212\/\u0394\n                      <jats:italic>vav<\/jats:italic>\n                    <\/jats:sup>\n                    mice induced systemic apoptosis of lymphocytes in the thymus, spleen and lymph nodes that was dependent on the presence of IL\u20106. IL\u20106 deficiency prolonged survival of\n                    <jats:italic>SOCS3<\/jats:italic>\n                    <jats:sup>\n                      \u2212\/\u0394\n                      <jats:italic>vav<\/jats:italic>\n                    <\/jats:sup>\n                    mice and ameliorated spontaneous inflammatory disease developing during adult life. Infection of\n                    <jats:italic>SOCS3<\/jats:italic>\n                    <jats:sup>\n                      \u2212\/\u0394\n                      <jats:italic>vav<\/jats:italic>\n                    <\/jats:sup>\n                    mice with LCMV induced a lethal inflammatory response that was dependent on IL\u20106, despite\n                    <jats:italic>SOCS3<\/jats:italic>\n                    <jats:sup>\n                      \u2212\/\u0394\n                      <jats:italic>vav<\/jats:italic>\n                    <\/jats:sup>\n                    mice controlling viral replication. We conclude that SOCS3 is required for survival during inflammatory responses and is a critical regulator of IL\u20106\n                    <jats:italic>in vivo<\/jats:italic>\n                    .\n                  <\/jats:p>","DOI":"10.1038\/icb.2011.29","type":"journal-article","created":{"date-parts":[[2011,4,26]],"date-time":"2011-04-26T05:39:36Z","timestamp":1303796376000},"page":"124-129","source":"Crossref","is-referenced-by-count":41,"title":["IL\u20106 promotes acute and chronic inflammatory disease in the absence of SOCS3"],"prefix":"10.1111","volume":"90","author":[{"given":"Ben A","family":"Croker","sequence":"first","affiliation":[{"name":"Department of Inflammation, The Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade  Parkville Victoria Australia"},{"name":"Department of Medical Biology, The University of Melbourne  Parkville Victoria 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Medical Research, 1G Royal Parade  Parkville Victoria Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Simon","family":"Preston","sequence":"additional","affiliation":[{"name":"Department of Infection and Immunity Divisions, The Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade  Parkville Victoria Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Donald","family":"Metcalf","sequence":"additional","affiliation":[{"name":"Department of Medical Biology, The University of Melbourne  Parkville Victoria Australia"},{"name":"Department of Cancer and Haematology, The Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade  Parkville Victoria Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joanne A","family":"O'Donnell","sequence":"additional","affiliation":[{"name":"Department of Medical Biology, The University of Melbourne  Parkville Victoria Australia"},{"name":"Department of Cancer and Haematology, The Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade  Parkville Victoria Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Louise H","family":"Cengia","sequence":"additional","affiliation":[{"name":"Department of Cancer and Haematology, The Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade  Parkville Victoria Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kate","family":"McArthur","sequence":"additional","affiliation":[{"name":"Department of Medical Biology, The University of Melbourne  Parkville Victoria Australia"},{"name":"Department of Cancer and Haematology, The Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade  Parkville Victoria Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicos A","family":"Nicola","sequence":"additional","affiliation":[{"name":"Department of Medical Biology, The University of Melbourne  Parkville Victoria 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