Abstract
Excessive complement activation significantly contributes to the pathogenesis of a large number of inflammatory diseases, including ischemia/reperfusion injury, sepsis, and multiple organ failure syndrome. Current strategies to interfere with the deleterious action of complement include the application of endogenous soluble complement inhibitors (C1 inhibitor, recombinant soluble complement receptor 1-rsCR1), administration of antibodies, blocking key proteins of the cascade reaction (e.g., C5), neutralizing the action of the complement-derived anaphylatoxin C5a, or interfering with complement receptor 3 (CR3, CD18/11b)-mediated adhesion of inflammatory cells to the vascular endothelium. Incorporation of membrane-bound complement regulators (DAF-CD55, MCP-CD46, CD59) has provided a major step forward in protecting xenografts from hyperacute rejection. Numerous animal studies and first clinical trials strongly suggest that complement inhibition is a suitable novel therapeutic approach to preventing inflammatory disorders.
Keywords
- Acute Pancreatitis
- Complement System
- Complement Inhibition
- Hyperacute Rejection
- Complement Control Protein
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Jurianz, K., Kirschfink, M. (2000). Therapeutic Complement Inhibition. In: Baue, A.E., Faist, E., Fry, D.E. (eds) Multiple Organ Failure. Springer, New York, NY. https://doi.org/10.1007/978-1-4612-1222-5_23
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