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The murine complement regulator Crry: new insights into the immunobiology of complement regulation
Authors:H Molina
Institution:(1) Veteran's Administration Medical Center, St. Louis, Missouri 63106 (USA); the Division of Rheumatology, Department of Medicine, and Department of Pathology, Washington University School of Medicine, Box 8045, 660 South Euclid Aventue, St. Louis, Missouri 63110 (USA), Fax +1 314 454 1091, e-mail: hmolina@imgate.wustl.edu, US
Abstract:Complement has an important role in inflammation and in the normal function of the immune system. Activated complement fragments have the capacity to bind and damage self-tissues. Cells from vertebrates express on their surface regulators of complement activation that protect them from the deleterious effects of cell-bound complement fragments. Abnormalities in these regulators of complement activation may participate in the pathogenesis of autoimmune diseases and inflammatory disorders. Murine Crry is one of these regulators that inhibits the activation of the third component of complement and protects self-tissues from complement-mediated damage. Experimental work on Crry has increased our understanding of the immunobiology of complement regulation and the potential role of complement and complement inhibitors in the development and treatment of human diseases. Received 13 June 2001; received after revision 12 July 2001; accepted 9 August 2001
Keywords:, Complement, complement regulators, C3, inflammation, transgenic mice, gene-targeted mice,
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