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.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
References
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.
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.
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.
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.
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.
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.
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.
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.
Wisnieski J. J. and Naff G. B. (1989) Serum IgG antibodies to Clq in hypocomplementemic urticarial vasculitis syndrome. Arth. Rheum. 32, 1119–1127.
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.
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.
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.
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.
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.
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.
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.
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.
Davies A.E. (1988) Cl inhibitor and hereditary angioneurotic edema. Ann. Rev.Immunol. 6, 595–628.
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.
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.
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.
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.
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.
Alsenz J., Bork K., and Loos M. (1987) Autoantibody-mediated acquired deficiency of Cl inhibitor. N. Engl J. Med. 316, 1360–1366.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
Laemmli U. K. (1970) Cleavage of structural proteins during the assembly of the head of bacteriophage T4. Nature 227, 680–686.
Author information
Authors and Affiliations
Editor information
Editors and Affiliations
Rights 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