Advertisement

Complement

  • A. G. Bird
Part of the Handbook of Experimental Pharmacology book series (HEP, volume 87 / 1)

Abstract

Complement is a system of factors occurring in blood and tissue fluids that are activated characteristically by antibody-antigen interactions. The consequences of the activation of complement are the release of products which mediate a number of biologically significant events. In common with other major humoral effector systems, including the clotting, kinin and fibrinolytic systems, complement is composed of a series of discrete proteins present as precursor molecules. These, when activated by a variety of stimuli, result in a reaction sequence which proceeds in a predefined direction. Complement, like the other triggered enzyme systems, displays the inherent amplification kinetics of a chain reaction and each protein product becomes a catalyst for the next in sequence. The net result is a cascade phenomenon during which intermediate proteins and breakdown products possessing potent biological activity are produced. The whole system is under stringent internal control and regulation, but initial activation produces a rapid local inflammatory response at the activation site. The products of complement activation comprise all the major functions necessary for acute inflammation and their release in vasodilatation, increased capillary permeability, neutrophil chemotaxis and subsequent particle phagocytosis.

Keywords

Systemic Lupus Erythematosus Immune Complex Complement Activation Bullous Pemphigoid Classical Pathway 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. Agnello V (1978) Complement deficiency states. Medicine 57:1–23PubMedCrossRefGoogle Scholar
  2. Berry DM, Almeida JD (1968) The morphological and biological effects of various antisera on avian infectious bronchitis virus. J Gen Virol 3:97–105PubMedCrossRefGoogle Scholar
  3. Bird P, Friedmann PS, Ling N, Bird AG, Thompson RA (1986) Subclass distribution of IgG autoantibodies in bullous pemphigoid. J Invest Dermatol 86:21–25PubMedCrossRefGoogle Scholar
  4. Cooper NR, Müller-Eberhard HJ (1967) Molecular measurement of the fourth component of human complement. In: Peeters H (ed) 15th Colloquium of Pro tides of the Biological Fluids. Elsevier, Amsterdam, pp 453–457Google Scholar
  5. Craddock PR, Hammerschmidt D, White JG, Dalmass AP, Jacob HS (1977) Complement (C5a) induced granulocyte aggregation in vitro. J Clin Invest 60:260–264PubMedCrossRefGoogle Scholar
  6. Donaldson VH, Hess EV, McAdams AJ (1977) Lupus erythematosus-like disease in three unrelated women with hereditary angio-neurotic oedema. Ann Intern Med 86:312–313PubMedGoogle Scholar
  7. Fearon DT (1984) Cellular receptors for fragments of the third component of complement. Immunology Today 5:105–110CrossRefGoogle Scholar
  8. Fielder AHL, Walport MJ, Batchelor JR, Rynes RJ, Black CM, Dodi IA, Hughes GRV (1983) A family study of the MHC of patients with SLE. Null alleles of C4A and C4B may determine disease susceptibility. Br Med J [Clin Res] 286:425–428CrossRefGoogle Scholar
  9. Fingeroth JD, Weiss JJ, Tedder TF, Strominger JL, Biro PA, Fearon DT (1984) Epstein-Barr virus receptor of human B lymphocytes is the C3d receptor CR2. Proc Natl Acad Sci USA 81:4510–4514PubMedCrossRefGoogle Scholar
  10. Fujita T, Takata Y, Tamura N (1981) Solubilisation of immune precipitates by six isolated alternative pathway proteins. J Exp Med 154:1743–1751PubMedCrossRefGoogle Scholar
  11. Gelfand JA, Sherin RJ, Ailing DW, Frank MM (1976) Treatment of hereditary angiooedema with danazol. N Engl J Med 295:1444–1448PubMedCrossRefGoogle Scholar
  12. Hammarschmidt DE, Weaver LJ, Hudson LD, Craddock PR, Jacob HS (1980) Association of complement activation and elevated plasma C5a with adult respiratory distress syndrome: pathophysiological relevance and possible prognostic value. Lancet 1:947–949CrossRefGoogle Scholar
  13. Hashimoto K, Shafran KM, Webber PS, Lazarus GS, Singer KH (1983) Anti-cell surface pemphigus autoantibody stimulates plasminogen activator activity of human epidermal cells. J Exp Med 157:259–272PubMedCrossRefGoogle Scholar
  14. Jordon RE, Heine KG, Tappeiner G, Bushkell LL, Provost TT (1976) The immunopathology of herpes gestationis: immunofluorescence studies and chracterisation of “HG factor”. J Clin Invest 57:1426–1431PubMedCrossRefGoogle Scholar
  15. Kazatchkine MD, Nydegger UE (1982) The human alternative pathway: biology and immunopathology of activation and regulation. Prog Allergy 30:193–234PubMedGoogle Scholar
  16. Klaus GGB, Humphrey JH (1977) The generation of memory cells. I. The role of C3 in the generation of B memory cells. Immunology 33:31–45PubMedGoogle Scholar
  17. Lachmann PJ, Rosen FS (1978) Genetic defects of complement in man. Springer Semin Immunopathol 1:107–119CrossRefGoogle Scholar
  18. Miller GW, Nussenzweig V (1975) A new complement function: solubilisation of antigen-antibody aggregates. Proc Natl Acad Sci USA 72:418–422PubMedCrossRefGoogle Scholar
  19. Müller-Eberhard HJ (1975) Complement. Annu Rev Biochem 44:697–715PubMedCrossRefGoogle Scholar
  20. Porter RR (1977) Structure and activation of the early components of complement. Fed Proc 36:2191–2196PubMedGoogle Scholar
  21. Porter RR (1983) Complement polymorphism, the major histocompatibility complex and associated diseases: a speculation. Mol Biol Med 1:161–168PubMedGoogle Scholar
  22. Provost TT, Tomasi TB (1974) Evidence for activation of complement via the alternative pathway in skin diseases. II. Dermatitis herpetiformis. Clin Immunol Immunopathol 3:178–186PubMedCrossRefGoogle Scholar
  23. Ruddy S (1980) Function of the control proteins of the classical and alternative complement activation pathways. In: Thompson RA (ed) Recent advances in clinical immunology, vol 2. Churchill Livingstone, Edinburgh, pp 91–111Google Scholar
  24. Schreiber AD, Kaplan AP, Austen KF (1973) Inhibition of C\(\bar 1\) INH of Hageman factor fragment activation of coagulation, fibrinolysis and kinin-generation. J Clin Invest 52:1402–1409PubMedCrossRefGoogle Scholar
  25. Unsworth DJ, Payne AW, Leonard JN, Fry L, Holborow EJ (1982) The IgA in dermatitis herpetiformis is dimeric. Lancet 1:478–480PubMedCrossRefGoogle Scholar
  26. Yefenof E, Klein G (1977) Membrane receptor stripping confirms the association between EBV receptors and complement receptors on the surface of human B lymphoma lines. Int J Cancer 20:347–352PubMedCrossRefGoogle Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 1989

Authors and Affiliations

  • A. G. Bird

There are no affiliations available

Personalised recommendations