{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,4]],"date-time":"2026-05-04T20:57:25Z","timestamp":1777928245849,"version":"3.51.4"},"reference-count":81,"publisher":"SAGE Publications","issue":"4","license":[{"start":{"date-parts":[[2009,3,10]],"date-time":"2009-03-10T00:00:00Z","timestamp":1236643200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Lupus"],"published-print":{"date-parts":[[2009,4]]},"abstract":"<jats:p>\n                    Tissue damage associated with a severe injury can result in profound inflammatory responses that may trigger autoimmune development in lupus-prone individuals. In this study, we investigated the role of a large full-thickness cutaneous burn injury on the early onset of autoimmune disease in lupus-prone MRL\/++ mice. MRL\/++ mice (chronic model) exhibit autoimmune symptoms at &gt;70\u00a0weeks of age, whereas MRL\/-Fas\n                    <jats:sup>lpr<\/jats:sup>\n                    mice (acute model) develop autoimmune disease in 17\u201322\u00a0weeks due to a lymphoproliferative mutation. Autoimmune disease developed in MRL\/++ mice (4\u201315\u00a0weeks post injury) is manifested by skin lesions, vasculitis, epidermal ulcers, cellular infiltration, splenomegaly, lymphadenopathy, hypergammaglobulinemia, elevated autoantibodies and renal pathologies including proteinuria, glomerulonephritis and immune complex deposition; complications that contribute to reduced survival. Transcription studies of wound margin tissue show a correlation between the pathogenic effects of dysregulated IL-1\u03b2, IL-6, TNF-\u03b1 and PGE\n                    <jats:sub>2<\/jats:sub>\n                    synthesis during early wound healing and early onset of autoimmune disease. Interestingly, MRL\/++ mice with healed wounds (30\u201340\u00a0days post burn) strongly rejected skin isografts. Conversely, skin isografts transplanted onto naive age-matched MRL\/++ littermates achieved long-term survival. Collectively, these findings suggest that traumatic injury exacerbates inflammatory skin disease and severe multi-organ pathogenesis in lupus-prone mice.\n                  <\/jats:p>","DOI":"10.1177\/0961203308097479","type":"journal-article","created":{"date-parts":[[2009,3,10]],"date-time":"2009-03-10T12:35:19Z","timestamp":1236688519000},"page":"318-331","source":"Crossref","is-referenced-by-count":22,"title":["Severe tissue trauma triggers the autoimmune state systemic lupus erythematosus in the MRL\/++ lupus-prone mouse"],"prefix":"10.1177","volume":"18","author":[{"given":"K","family":"Anam","sequence":"first","affiliation":[{"name":"Regenerative Medicine Department, Naval Medical Research Center, Silver Spring, Maryland, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M","family":"Amare","sequence":"additional","affiliation":[{"name":"Regenerative Medicine Department, Naval Medical Research Center, Silver Spring, Maryland, 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