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.
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