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      The complement system: History, pathways, cascade and inhibitors

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          Abstract

          Since its discovery in the 19th century, the complement system has developed into a clinically significant entity. The complement system has been implicated in a variety of clinical conditions, from autoimmune diseases to ischemia-reperfusion injury in transplantation. This article charts the historical progress of our understanding of the complement system and provides a synopsis on the activation pathways and its inherent regulators.

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          Complement. Second of two parts.

          M J Walport (2001)
          Article 0 comments Cited 303 times – based on 0 reviews     Review now
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            Complement control protein factor H: the good, the bad, and the inadequate.

            Viviana Ferreira, Michael Pangburn, Claudio Cortés (2010)
            The complement system is an essential component of the innate immune system that participates in elimination of pathogens and altered host cells and comprises an essential link between the innate and adaptive immune system. Soluble and membrane-bound complement regulators protect cells and tissues from unintended complement-mediated injury. Complement factor H is a soluble complement regulator essential for controlling the alternative pathway in blood and on cell surfaces. Normal recognition of self-cell markers (i.e. polyanions) and C3b/C3d fragments is necessary for factor H function. Inadequate recognition of host cell surfaces by factor H due to mutations and polymorphisms have been associated with complement-mediated tissue damage and disease. On the other hand, unwanted recognition of pathogens and altered self-cells (i.e. cancer) by factor H is used as an immune evasion strategy. This review will focus on the current knowledge related to these versatile recognition properties of factor H. Copyright 2010 Elsevier Ltd. All rights reserved.
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              Interaction between the coagulation and complement system.

              U Brückner, Daniel Rittirsch, Daniel Rittirsch … (2008)
              The complement system as a main column of innate immunity and the coagulation system as a main column in hemostasis undergo massive activation early after injury. Interactions between the two cascades have often been proposed but the precise molecular pathways of this interplay are still in the dark. To elucidate the mechanisms involved, the effects of various coagulation factors on complement activation and generation of anaphylatoxins were investigated and summarized in the light of the latest literature. Own in vitro findings suggest, that the coagulation factors FXa, FXIa and plasmin may cleave both C5 and C3, and robustly generate C5a and C3a (as detected by immunoblotting and ELISA). The produced anaphylatoxins were found to be biologically active as shown by a dose-dependent chemotactic response of neutrophils and HMC-1 cells, respectively. Thrombin did not only cleave C5 (Huber-Lang et al. 2006) but also in vitro-generated C3a when incubated with native C3. The plasmin-induced cleavage activity could be dose-dependently blocked by the serine protease inhibitor aprotinin and leupeptine. These findings suggest that various serine proteases belonging to the coagulation system are able to activate the complement cascade independently of the established pathways. Moreover, functional C5a and C3a are generated, both of which are known to be crucially involved in the inflammatory response.
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                Author and article information

                Journal
                Journal ID (publisher-id): 1886
                Journal ID (MPID): 122234
                Title: European Journal of Microbiology and Immunology
                Publisher: Akadémiai Kiadó
                ISSN (Print): 2062-509X
                ISSN (Electronic): 2062-8633
                Publication date (Print): 1 June 2012
                Publication date (Electronic): 13 June 2012
                Volume: 2
                Issue: 2 ( otherID: K022535X4502 )
                Pages: 103-111
                Affiliations
                [ 1 ] University Hospital of Wales Cardiff Transplant Unit Cardiff UK
                [ 2 ] Cardiff University Institute of Molecular and Experimental Medicine, School of Medicine Cardiff UK
                [ 3 ] University Hospital of Wales Dept of Transplant Surgery Cardiff CF10 5NQ UK
                Article
                Other ID: Y3705X045521K22N
                DOI: 10.1556/EuJMI.2.2012.2.2
                SO-VID: 73afb235-4c8d-48cd-84f5-f2276bb6cf78
                History
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                Subject: Review Articles

                ScienceOpen disciplines: Medicine,Immunology,Health & Social care,Microbiology & Virology,Infectious disease & Microbiology
                Keywords: complement inhibitors,complement history,complement cascade,complement system,complement activation
                Data availability:
                ScienceOpen disciplines: Medicine, Immunology, Health & Social care, Microbiology & Virology, Infectious disease & Microbiology
                Keywords: complement inhibitors, complement history, complement cascade, complement system, complement activation

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