Molecular Regulation of Complement Gene Expression

  • Harvey R. Colten
Part of the Veröffentlichungen aus der Geomedizinischen Forschungsstelle der Heidelberger Akademie der Wissenschaften book series (HD AKAD, volume 1987/88 / 1987/4)


The complement system consists of a group of more than 20 proteins that initiate and amplify antimicrobial host defense mechanisms mediated by the inflammatory response. The early acting proteins of the complement cascade and several proteins that function in control of complement activation are synthesized in hepatocytes and in extrahepatic tissues in mononuclear phagocytes. Differential regulation of complement production at hepatic and extrahepatic sites permits independent control of the size of the complement reservoir in plasma and the local concentration of these proteins at local tissue sites of inflammation. The effect of this selective control is illustrated in recent studies of endotoxin, interleukin-l, tumor necrosis factor and IFN-gamma modulation of complement gene expression. The mechanisms involved in cytokine regulation of these genes are relevant to the molecular iinnunobiology of specific immune responses, as well as to the regulation of inflammation. Many of these studies are reviewed in the references.


Mononuclear Phagocyte Extrahepatic Site Antimicrobial Host Defense Albumin Expression Primary Human Cell Culture 
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  1. Carroll MC, Campbell RD, Bentley D, Porter RR. A molecular map of the major histocompatibility class III region of man linking the complement genes C4, C2 and factor B. Nature 1984; 307: 237–240.PubMedCrossRefGoogle Scholar
  2. Chaplin DD, Woods DE, Whitehead AS, Goldberger G, Colter HR, Seidman JG. Molecular map of the marine S region. Proc Natl Acad Sci USA 1983; 80: 6947–6951.PubMedCrossRefGoogle Scholar
  3. Perlmutter DH, Colten HR. Molecular immunobiology of complement biosynthesis: A model of single cell control of effector-inhibitor balance. Ann Rev Inmunol 1986; 4: 231–251.CrossRefGoogle Scholar
  4. Perlmutter DH, Colten HR, Grossberger D, Strominger J, Seidman JG, Chaplin DD. Expression of complement proteins C2 and factor B in transfected L-cells. J Clin Invest 1985; 76: 1449–1454.PubMedCrossRefGoogle Scholar
  5. Perlmutter DH, Goldberger G, Dinarello CA, Mizel SB, Colten HR. Regulation of class III major histocompatibility complex (IHC) gene products by interleukin1. Science 1986; 232: 850–852.PubMedCrossRefGoogle Scholar
  6. Ramadori JG, Sipe JD, Colten HR. Expression and regulation of the murine serum amyloid A (SAA) gene in extrahepatic sites. J Iir¢nunol 1985; 135: 3645–3647.Google Scholar
  7. Ramadori G, Sipe JD, Dinarello CA, Mizel SB, Colten HR. Pretranslational modulation of acute phase hepatic protein synthesis by murine recombinant interleukin 1 (IL-1) and purified human IL-1. J Exp Ned 1985; 162: 930–942.Google Scholar
  8. Strunk RC, Cole FS, Perlmutter DH, Colten HR. Gamma-interferon increases expression of class III clement genes C2 and factor B in human monocytes and in marine fibroblasts transfected with human C2 and factor B genes. J Biol Chem 1985; 260: 15280–15285.PubMedGoogle Scholar
  9. Strunk RC, Whitehead AS, Cole FS. Pretranslational regulation of the synthesis of the third component of complement in human mononuclear phagocytes by the lipid A portion of lipopolysaccharide. J Clin Invest 1985; 76: 985–990.PubMedCrossRefGoogle Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 1987

Authors and Affiliations

  • Harvey R. Colten
    • 1
  1. 1.Department of PediatricsWashington University School of MedicineSt. LouisUSA

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