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      Overview of Complement Activation and Regulation

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          Summary

          Complement is an important component of the innate immune system that is crucial for defense from microbial infections and for clearance of immune complexes and injured cells. In normal conditions complement is tightly controlled by a number of fluid-phase and cell surface proteins to avoid injury to autologous tissues. When complement is hyperactivated, as occurs in autoimmune diseases or in subjects with dysfunctional regulatory proteins, it drives a severe inflammatory response in numerous organs. The kidney appears to be particularly vulnerable to complement-mediated inflammatory injury. Injury may derive from deposition of circulating active complement fragments in glomeruli, but complement locally produced and activated in the kidney also may have a role. Many kidney disorders have been linked to abnormal complement activation, including immune-complex–mediated glomerulonephritis and rare genetic kidney diseases, but also tubulointerstitial injury associated with progressive proteinuric diseases or ischemia-reperfusion.

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          Atypical hemolytic-uremic syndrome.

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            Complement. Second of two parts.

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              Role of C5a in inflammatory responses.

              The complement system not only represents an effective innate immune mechanism of host defense to eradicate microbial pathogens, but it is also widely involved in many forms of acute and chronic inflammatory diseases including sepsis, acute lung injury, ischemia-reperfusion injury, and asthma, to give just a few examples. The complement-activated product, C5a, displays powerful biological activities that lead to inflammatory sequelae. C5a is a strong chemoattractant and is involved in the recruitment of inflammatory cells such as neutrophils, eosinophils, monocytes, and T lymphocytes, in activation of phagocytic cells and release of granule-based enzymes and generation of oxidants, all of which may contribute to innate immune functions or tissue damage. Accumulating data suggest that C5a provides a vital bridge between innate and adaptive immune functions, extending the roles of C5a in inflammation. Herein, we review human and animal data describing the cellular and molecular mechanisms of C5a in the development of inflammatory disorders, sepsis, acute lung injury, ischemia-reperfusion injury, and asthma.
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                Author and article information

                Contributors
                Journal
                Semin Nephrol
                Semin. Nephrol
                Seminars in Nephrology
                W.B. Saunders
                0270-9295
                1558-4488
                1 November 2013
                November 2013
                : 33
                : 6
                : 479-492
                Affiliations
                IRCCS- Istituto di Ricerche Farmacologiche “Mario Negri”, Bergamo, Italy
                Author notes
                [* ]Address reprint requests to Marina Noris, PhD, Istituto di Ricerche Farmacologiche “Mario Negri,” IRCCS, Clinical Research Center for Rare Diseases “Aldo e CeleDaccò,” ViaCamozzi, 3–24020 Ranica, Bergamo, Italy marina.noris@ 123456marionegri.it
                Article
                S0270-9295(13)00129-0
                10.1016/j.semnephrol.2013.08.001
                3820029
                © 2013 Elsevier Inc.

                This document may be redistributed and reused, subject to certain conditions.

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