Skip to main content

Autoantibodies to Complement Components

  • Protocol
Complement Methods and Protocols

Part of the book series: Methods in Molecular Biology ((MIMB,volume 150))

Abstract

The purpose of the immune system is to defend the host from constantly changing microbial pathogens. Autoimmune diseases develop as a consequence of the production of antibodies and/or cells that react with self-antigens, and may recmit other effector mechanisms that result in tissue damage. Thus, in this context, autoimmunity represents an immune response to self-antigens that is sufficient to cause disease. It should not be forgotten that apparently harmless autoantibodies may also be formed following tissue damage (e.g.. antiheart antibodies, after a myocardial infarction), and the evidence that many of the autoantibodies routinely measured in the laboratory are directly pathogenic, is weak.

This is a preview of subscription content, log in via an institution to check access.

Access this chapter

Protocol
USD 49.95
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
eBook
USD 129.00
Price excludes VAT (USA)
  • Available as EPUB and PDF
  • Read on any device
  • Instant download
  • Own it forever
Softcover Book
USD 169.99
Price excludes VAT (USA)
  • Compact, lightweight edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info
Hardcover Book
USD 169.99
Price excludes VAT (USA)
  • Durable hardcover edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info

Tax calculation will be finalised at checkout

Purchases are for personal use only

Institutional subscriptions

References

  1. Antes U., Heinz H. P., and Loos M. (1988) Evidence for the presence of autoantibodies to the collagen-like portion of Clq in systemic lupus erythematosus. Arth.Rheum. 31, 457–464.

    Article  CAS  Google Scholar 

  2. Golan M. D., Burger R., and Loos M. (1982) Conformational changes in Clq after binding to immune complexes: detection of neoantigens with monoclonal antibodies. J. Imrrumol 129, 445–447.

    CAS  Google Scholar 

  3. Hoekzema R., Martens M., Brouwer M. C, and Hack C. E. (1988) The distortive mechanism for the activation of complement component Cl supported by studies with a monoclonal antibody against the “arms” of Clq. Mol. Immunol. 25, 485–494.

    Article  PubMed  CAS  Google Scholar 

  4. Wener M. H., Uwatoko S., and Mannik M. (1989) Antibodies to the collagenlike region of Clq in sera of patients with autoimmune rheumatic diseases. Arth.Rheum. 32, 544–551.

    Article  CAS  Google Scholar 

  5. Prada A.E. and Strife C. F. (1992) IgG subclass restriction of autoantibody to solid-phase Clq in membranoproliferative and lupus glomerulonephritis. Clin.Immunol Immunopathol. 63, 84–88.

    Article  PubMed  CAS  Google Scholar 

  6. Strife C. F., Leahy A. E., and West C. D. (1989) Antibody to a cryptic, solid phase C1Q antigen in membranoproliferative nephritis. Kidney Int. 35, 836–842.

    Article  PubMed  CAS  Google Scholar 

  7. Siegert C.E., Daha M.R., van derVoort E.A.,and Breedveld F.C. (1990) IgG and IgA antibodies to the collagen-like region of Clq in rheumatoid vasculitis. Arth. Rheum 33, 1646–1654.

    Article  CAS  Google Scholar 

  8. Marder R. J., Potempa L. A., Jones J. V., Toriumi D., Schmid F. R., and Gewurz H. (1984) Assay, purification and further characterization of 7S Clq precipitins (Clq-p) in hypocomplementemic vasculitis urticaria syndrome and systemic lupus erythematosus. Acta PathoL Microbiol. Immunol. Scand. Suppl. 284, 25–34.

    PubMed  CAS  Google Scholar 

  9. Wisnieski J. J. and Naff G. B. (1989) Serum IgG antibodies to Clq in hypocomplementemic urticarial vasculitis syndrome. Arth. Rheum. 32, 1119–1127.

    Article  CAS  Google Scholar 

  10. Siegert C. E., Daha M. R., Halma C, van der Voort E. A., and Breedveld F. C. (1992) IgG and IgA autoantibodies to Clq in systemic and renal diseases. Clin.Exp. Rheumatol. 10, 19–23.

    PubMed  CAS  Google Scholar 

  11. Coremans I. E., Daha M. R., van der Voort E. A., Muizert Y., Halma C, and Breedveld F. C. (1992) Antibodies against Clq in anti-glomerular basement membrane nephritis. Clin. Exp. Immunol. 87, 256–260.

    Article  PubMed  CAS  Google Scholar 

  12. Siegert C., Daha M., Westedt M. L., van der Voort E., and Breedveld F. (1991) IgG auto antibodies against Clq are correlated with nephritis, hypocomplementemia, and dsDNA antibodies in systemic lupus erythematosus. J. Rheumatol. 18, 230–234.

    PubMed  CAS  Google Scholar 

  13. Uwatoko S., Aotsuka S., Okawa M., Egusa Y., Yokohari R., Aizawa C. and Suzuki K. (1987) Clq solid-phase radioimmunoassay: evidence for detection of antibody directed against the collagen-like region of Clq in sera from patients with systemic lupus erythematosus. Ciin. Exp. Immunol. 69, 98–106.

    CAS  Google Scholar 

  14. Siegert C. E., Daha M. R., Tseng C. M., Coremans I. E., van Es L. A., and Breedveld F. C. (1993) Predictive Ann. Rheum. Dis.value of IgG autoantibodies against Clq for nephritis in systemic lupus erythematosus. Ann. Rheum. Dis. 52, 851–856.

    Article  PubMed  CAS  Google Scholar 

  15. Coremans I. E., Spronk P. E., Bootsma H., Daha M. R., van der Voort E. A., Kater L., Breedveld F. C, and Kallenberg C. G. (1995) Changes in antibodies to Clq predict renal relapses in systemic lupus erythematosus. Am. J. Kidney Dis. 26, 595–601.

    Article  PubMed  CAS  Google Scholar 

  16. Norsworthy P., Theodoridis E., Botto M., Athanassiou P., Beynon H., Gordon C. et al. (1999) Over-representation of the FcyRIIA R131/131 genotype in caucasoid SLE patients with auto-antibodies to Clq and glomerulonephritis. Arth. Rheum. 42, 1828–1832.

    Article  CAS  Google Scholar 

  17. Wisnieski J. J., Baer A. N., Christensen J., Cupps T. R., Flagg D. N., Jones J. V., et al. (1995) Hypocomplementemic urticarial vasculitis syndrome. Clinical and serologic findings in 18 patients. Med. Bat. 74, 24–41.

    Article  CAS  Google Scholar 

  18. Davies A.E. (1988) Cl inhibitor and hereditary angioneurotic edema. Ann. Rev.Immunol. 6, 595–628.

    Article  Google Scholar 

  19. Cicardi M., Beretta A., Colombo M., Gioffre D., Cugno M., and Agostoni A. (1996) Relevance of lympho proliferative disorders and of anti-Cl inhibitor autoantibodies in acquired angio-oedema. Ciin. Exp. Immunol. 106, 475–480.

    Article  CAS  Google Scholar 

  20. Geha R. S., Quinti I., Austen K. F., Cicardi M., Sheffer A., and Rosen F. S. (1985) Acquired Cl-inhibitor deficiency associated with antiidiotypic antibody to monoclonal immunoglobulins. N. Engl. J. Med. 312, 534–540.

    Article  PubMed  CAS  Google Scholar 

  21. Malbran A., Hammer C. H., Frank M. M., and Fries L. F. (1988) Acquired angioedema: observations on the mechanism of action of autoantibodies directed against Cl esterase inhibitor. J. Aller. Ciin. Immunol. 81, 1199–1204.

    Article  CAS  Google Scholar 

  22. Mandle R., Baron C, Roux E., Sundel R., Gelfand J., Aulak K., et al. (1994) Acquired Cl inhibitor deficiency as a result of an autoantibody to the reactive center region of Cl inhibitor. J. Immunol. 152, 4680–4685.

    PubMed  CAS  Google Scholar 

  23. He S., Tsang S., North J., Chohan N., Sim R.B., and Whaley K. (1996) Epitope mapping of Cl inhibitor autoantibodies from patients with acquired Cl inhibitor deficiency. J. Immunol. 156, 2009–2013.

    PubMed  CAS  Google Scholar 

  24. Alsenz J., Bork K., and Loos M. (1987) Autoantibody-mediated acquired deficiency of Cl inhibitor. N. Engl J. Med. 316, 1360–1366.

    Article  PubMed  CAS  Google Scholar 

  25. Spitzer R.E., Vallota E.H., Forristal J., Sudora E., Stitzel A., Davis N. C, and West C. D. (1969) Serum C’3 lytic system in patients with glomerulonephritis. Science 164, 436–437.

    Article  PubMed  CAS  Google Scholar 

  26. Peters D. K., Charlesworth J. A., Sissons J. G., Williams D. G., Boulton Jones J. M., Evans D. J., et al. (1973) Mesangiocapillary nephritis, partial lipodystrophy, and hypocomplementaemia. Lancet 2, 535–538.

    Article  PubMed  CAS  Google Scholar 

  27. Vallota E. H., Forristal J., Spitzer R. E., Davis N. C, and West C. D. (1970) Characteristics of a non-complement-dependent C3-reactive complex formed form factors in nephritic and normal serum. J. Exp. Med. 131, 1306–1324.

    Article  PubMed  CAS  Google Scholar 

  28. Vallota E. H., Forristal J., Spitzer R. E., Davis N. C, and West C. D. (1971) Continuing C3 breakdown after bilateral nephrectomy in patients with membranoproliferative glomerulonephritis. J. Clin. Invest. 50, 552–558.

    Article  PubMed  CAS  Google Scholar 

  29. Daha M.R., Fearon D.T., and Austen K.F. (1976) C3 nephritic factor (C3NeF): stabilization of fluid phase and cell-bound alternative pathway convertase. J.Immunol. 116, 1–7.

    PubMed  CAS  Google Scholar 

  30. Weiler J. M., Daha M. R., Austen K. F., and Fearon D. T. (1976). Control of the amplification convertase of complement by the plasma protein betalH. Proc.Natl. Acad. Sci. USA 73, 3268–3272.

    Article  PubMed  CAS  Google Scholar 

  31. Tanuma Y., Ohi H., and Hatano M. (1990). Two types of C3 nephritic factor: properd in-dependent C3NeF and properdin-independent C3NeF. Clin. Immunol.Immunopathol. 56, 226–238.

    Article  PubMed  CAS  Google Scholar 

  32. Ohi H., Watanabe S., Fujita T., and Yasugi T. (1992) Significance of C3 nephritic factor (C3NeF) in non-hypocomplementaemic serum with membranoproliferative glomerulonephritis (MPGN). Clin. Exp. Immunol. 89, 479–484.

    Article  PubMed  CAS  Google Scholar 

  33. Daha M. R. and van Es L. A. (1981) Stabilization of homologous andheterologous cell-bound amplification convertases, C3bBb,by C3 nephritic factor. Immunology 43, 33–38.

    PubMed  CAS  Google Scholar 

  34. Halbwachs L., Leveille M., Lesavre P., Wattel S., and Leibowitch J. (1980) Nephritic factor of the classical pathway of complement: immunoglobulin G autoantibody directed against the classical pathway C3 convertase enzyme. J. Clin.Invest. 65, 1249–1256.

    Article  PubMed  CAS  Google Scholar 

  35. Daha M. R., Hazevoet H. M., Vanes L. A., and Cats A. (1980) Stabilization of the classical pathway C3 convertase C42, by a factor F-42, isolated from serum of patients with systemic lupus erythematosus. Immunology 40, 411–421.

    Google Scholar 

  36. Fujita T., Sumita T., Yoshida S., Ito S., and Tamura N. (1987) C4 nephritic factor in a patient with chronic glomerulonephritis. J. Clin. Lab. Immunol 22, 65–70.

    PubMed  CAS  Google Scholar 

  37. Tanuma Y, Ohi H., Watanabe S., Seki M., and Hatano M. (1989) C3 nephritic factor and C4 nephritic factor in the serum of two patients with hypocomplementaemic membranoproliferativeglomerulonephritis. Clin. Exp. Immunol 76, 82–85.

    PubMed  CAS  Google Scholar 

  38. Gigli I., Sorvillo J., and Halbwachs, Mecarelli L. (1985) Regulation and deregulation of the fluid-phase classical pathway C3 convertase. J. Immunol 135, 440–444.

    PubMed  CAS  Google Scholar 

  39. Ohi H. and Yasugi T. (1994) Occurrence of C3 nephritic factor and C4 nephritic factor in membranoproliferative glomerulonephritis (MPGN). Clin. Exp. Immunol. 95, 316–321.

    Article  PubMed  CAS  Google Scholar 

  40. Sakari Jokiranta T., Solomon A., Zipfei P. F., Pangburn M. K., and Meri S. (1996) Structure and function of a nephritogenic λ-light chain dimer—a unique human miniautoantibody against factor H. Mol. Immunol. 33, 11.

    Google Scholar 

  41. He H. and Lin Y-L. (1998) In vitro stimulation of Cls-presenting autoantibodies from patients with systemic lupus erythematosus. J. Immunol. 160, 4641–4647.

    PubMed  CAS  Google Scholar 

  42. Laemmli U. K. (1970) Cleavage of structural proteins during the assembly of the head of bacteriophage T4. Nature 227, 680–686.

    Article  PubMed  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Editor information

Editors and Affiliations

Rights and permissions

Reprints and permissions

Copyright information

© 2000 Humana Press Inc., Totowa, NJ

About this protocol

Cite this protocol

Davies, K.A., Norsworthy, P. (2000). Autoantibodies to Complement Components. In: Morgan, B.P. (eds) Complement Methods and Protocols. Methods in Molecular Biology, vol 150. Humana Press. https://doi.org/10.1385/1-59259-056-X:173

Download citation

  • DOI: https://doi.org/10.1385/1-59259-056-X:173

  • Publisher Name: Humana Press

  • Print ISBN: 978-0-89603-654-3

  • Online ISBN: 978-1-59259-056-8

  • eBook Packages: Springer Protocols

Publish with us

Policies and ethics