Loss of Autoantibody Activity by Alteration in Autoantigen

C3 nephritic factor (C3NeF) is an autoantibody produced by patients with membranoproliferative glomerulonephritis (MPGN); it is thought to be responsible for the continued breakdown of C3 in these patients. We have studied three patients with MPGN for periods of 7 to 17 years who were noted to devel...

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Bibliographic Details
Published in:Clinical immunology and immunopathology 1996-08, Vol.80 (2), p.211-213
Main Authors: Spitzer, Roger E., Stitzel, Ann E.
Format: Article
Language:English
Subjects:
Adult
Antigen-Antibody Reactions - drug effects
Autoantibodies - blood
Autoantibodies - metabolism
Autoantibodies - pharmacology
Autoantigens - blood
Autoantigens - immunology
Autoantigens - metabolism
Biological and medical sciences
Complement C3 - metabolism
Complement C3 Nephritic Factor - metabolism
Complement C3 Nephritic Factor - pharmacology
Complement Factor B - metabolism
Complement Factor B - pharmacology
Female
Glomerulonephritis
Glomerulonephritis, Membranoproliferative - immunology
Humans
Medical sciences
Nephrology. Urinary tract diseases
Nephropathies. Renovascular diseases. Renal failure
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Description
Summary:C3 nephritic factor (C3NeF) is an autoantibody produced by patients with membranoproliferative glomerulonephritis (MPGN); it is thought to be responsible for the continued breakdown of C3 in these patients. We have studied three patients with MPGN for periods of 7 to 17 years who were noted to develop a normal C3 and factor B level in the face of persistent circulating C3NeF. In addition, C3NeF obtained from other sera were inactive when added to these patients’ sera. When C3NeF was isolated from these patients’ sera, however, it was completely active when added to normal human serum as a source of C3 and factor B. Removal of the C3 and factor B from these patients’ sera by passage over anti-C3 and anti-factor B columns followed by reconstitution with C3 and factor B isolated from normal serum allowed C3NeF to be active in these sera. Replacement of C3 alone did not restore activity to these sera but replacement with factor B alone restored full C3NeF activity. These data suggest some alteration in autoantigen (factor B) as a mechanism for reduction in autoantibody (C3NeF) activity.
ISSN:0090-1229
1090-2341
DOI:10.1006/clin.1996.0116