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Accelerated Ischemia/Reperfusion-Induced Injury in Autoimmunity-Prone Mice^1,2

Sherry D. Fleming^*,, Marc Monestier and George C. Tsokos^3,*,

^* Department of Cellular Injury, Walter Reed Army Institute of Research, Silver Spring, MD 20910; Department of Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD 20814; and Department of Microbiology and Immunology, School of Medicine, Temple University, Philadelphia, PA 19140

Natural Abs have been implicated in initiating mesenteric ischemia/reperfusion (I/R)-induced tissue injury. Autoantibodies have affinity and self-Ag recognition patterns similar to natural Abs. We considered that autoimmunity-prone mice that express high titers of autoantibodies should have enhanced I/R-induced injury. Five-month-old B6.MRL/lpr mice displayed accelerated and enhanced intestinal I/R-induced damage compared with 2-mo-old B6.MRL/lpr and age-matched C57BL/6 mice. Similarly, older autoimmune mice had accelerated remote organ (lung) damage. Infusion of serum IgG derived from 5-mo-old but not 2-mo-old B6.MRL/lpr into I/R resistant Rag-1^–/– mice rendered them susceptible to local and remote organ injury. Injection of monoclonal IgG anti-DNA and anti-histone Abs into Rag-1^–/– mice effectively reconstituted tissue injury. These data show that like natural Abs, autoantibodies, such as anti-dsDNA and anti-histone Abs, can instigate I/R injury and suggest that they are involved in the development of tissue damage in patients with systemic lupus erythematosus.

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