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Tytuł:
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Loss of autoantibody activity by alteration in autoantigen.
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Autorzy:
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Spitzer RE; Department of Pediatrics, SUNY Health Science Center, Syracuse, New York 13210, USA.
Stitzel AE
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Źródło:
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Clinical immunology and immunopathology [Clin Immunol Immunopathol] 1996 Aug; Vol. 80 (2), pp. 211-3.
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Typ publikacji:
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Journal Article; Research Support, Non-U.S. Gov't
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Język:
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English
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Imprint Name(s):
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Publication: -1998: Orlando, FL : Academic Press
Original Publication: New York, Academic Press,
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MeSH Terms:
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Autoantibodies/*pharmacology
Autoantigens/*immunology
Autoantigens/*metabolism
Complement C3 Nephritic Factor/*pharmacology
Glomerulonephritis, Membranoproliferative/*immunology
Adult ; Antigen-Antibody Reactions/drug effects ; Autoantibodies/blood ; Autoantibodies/metabolism ; Autoantigens/blood ; Complement C3/metabolism ; Complement C3 Nephritic Factor/metabolism ; Complement Factor B/metabolism ; Complement Factor B/pharmacology ; Female ; Humans
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Substance Nomenclature:
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0 (Autoantibodies)
0 (Autoantigens)
0 (Complement C3)
0 (Complement C3 Nephritic Factor)
EC 3.4.21.47 (Complement Factor B)
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Entry Date(s):
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Date Created: 19960801 Date Completed: 19961001 Latest Revision: 20190821
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Update Code:
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20240104
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DOI:
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10.1006/clin.1996.0116
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PMID:
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8764567
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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.