{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T15:20:45Z","timestamp":1791300045877,"version":"4.1.0"},"reference-count":12,"publisher":"National Academy of Sciences","issue":"16","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2000,8]]},"abstract":"<jats:p>Mice lacking the gene encoding the suppressor of cytokine signaling-1 (SOCS-1 \u2212\/\u2212) and heterozygous for the IFN\u2013\u03b3 gene (IFN-\u03b3 +\/\u2212) avoided the IFN-\u03b3-dependent preweaning death of SOCS-1 \u2212\/\u2212 IFN-\u03b3 +\/+ mice but did not exhibit the good health of young adult SOCS-1 \u2212\/\u2212 IFN-\u03b3 \u2212\/\u2212 mice. SOCS-1 \u2212\/\u2212 IFN-\u03b3 +\/\u2212 mice died within 160 days of birth with massive T lymphocyte, macrophage, and eosinophil infiltration of all skeletal muscles and a similar severe myocarditis. The cornea also developed inflammatory infiltration and often a corneal ulcer. The mice exhibited evidence of selective CD8 T lymphocyte activation in populations in the thymus, spleen, and lymph nodes and focal T- and B-lymphoid infiltrates developed in the lung and salivary gland without apparent tissue damage. Comparison of SOCS-1 \u2212\/\u2212 IFN-\u03b3 +\/\u2212 mice with various control mice indicated that the development of tissue-damaging T lymphocyte, macrophage, and eosinophil infiltrates required loss of SOCS-1 and the presence of some IFN\u2013\u03b3, but that the lung lymphoid infiltrates required only loss of SOCS-1 to develop.<\/jats:p>","DOI":"10.1073\/pnas.160255197","type":"journal-article","created":{"date-parts":[[2002,7,26]],"date-time":"2002-07-26T10:41:48Z","timestamp":1027680108000},"page":"9174-9179","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":52,"title":["The development of fatal myocarditis and polymyositis in mice heterozygous for IFN-\u03b3 and lacking the SOCS-1 gene"],"prefix":"10.1073","volume":"97","author":[{"given":"Donald","family":"Metcalf","sequence":"first","affiliation":[{"name":"The Walter and Eliza Hall Institute of Medical Research and the Cooperative Research Centre for Cellular Growth 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