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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| Veröffentlicht in: | Clinical immunology and immunopathology 1996-08, Vol.80 (2), p.211-213 |
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| container_title | Clinical immunology and immunopathology |
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| creator | Spitzer, Roger E. Stitzel, Ann E. |
| description | 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. |
| doi_str_mv | 10.1006/clin.1996.0116 |
| format | Article |
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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.</description><identifier>ISSN: 0090-1229</identifier><identifier>EISSN: 1090-2341</identifier><identifier>DOI: 10.1006/clin.1996.0116</identifier><identifier>PMID: 8764567</identifier><identifier>CODEN: CLIIAT</identifier><language>eng</language><publisher>San Diego, CA: Elsevier Inc</publisher><subject>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</subject><ispartof>Clinical immunology and immunopathology, 1996-08, Vol.80 (2), p.211-213</ispartof><rights>1996 Academic Press</rights><rights>1996 INIST-CNRS</rights><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c399t-9cddb08b000099ebe36ec0e77900b37d4bc0969e8a00990f588abb5ffb1b94863</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=3139697$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8764567$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Spitzer, Roger E.</creatorcontrib><creatorcontrib>Stitzel, Ann E.</creatorcontrib><title>Loss of Autoantibody Activity by Alteration in Autoantigen</title><title>Clinical immunology and immunopathology</title><addtitle>Clin Immunol Immunopathol</addtitle><description>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.</description><subject>Adult</subject><subject>Antigen-Antibody Reactions - drug effects</subject><subject>Autoantibodies - blood</subject><subject>Autoantibodies - metabolism</subject><subject>Autoantibodies - pharmacology</subject><subject>Autoantigens - blood</subject><subject>Autoantigens - immunology</subject><subject>Autoantigens - metabolism</subject><subject>Biological and medical sciences</subject><subject>Complement C3 - metabolism</subject><subject>Complement C3 Nephritic Factor - metabolism</subject><subject>Complement C3 Nephritic Factor - pharmacology</subject><subject>Complement Factor B - metabolism</subject><subject>Complement Factor B - pharmacology</subject><subject>Female</subject><subject>Glomerulonephritis</subject><subject>Glomerulonephritis, Membranoproliferative - immunology</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Nephropathies. Renovascular diseases. Renal failure</subject><issn>0090-1229</issn><issn>1090-2341</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE1LxDAQhoMo67p69Sb0IN62TvqRJt6WxS9Y8KLnkKRTiXTbNUmF_fembNmbeMrA-8xk5iHkmkJKAdi9aW2XUiFYCpSyEzKnIGCZ5QU9JXMYa5pl4pxceP8FsaGAakZmvGJFyao5edj03id9k6yG0KsuWN3X-2Rlgv2xYZ_oWLcBnQq27xLbHbFP7C7JWaNaj1fTuyAfT4_v65fl5u35db3aLE0uRFgKU9cauI6fgxCoMWdoAKtKAOi8qgttQDCBXI05NCXnSuuyaTTVouAsX5C7w9yd678H9EFurTfYtqrDfvCy4rQss5L_C9KSU8GzEUwPoHHxeoeN3Dm7VW4vKcjRqhytytGqHK3Ghptp8qC3WB_xSWPMb6dceaPaxqnOWH_EcprHC0eMHzCMun4sOumNxc5gbR2aIOve_rXBL5e2kjw</recordid><startdate>19960801</startdate><enddate>19960801</enddate><creator>Spitzer, Roger E.</creator><creator>Stitzel, Ann E.</creator><general>Elsevier Inc</general><general>Academic Press</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>19960801</creationdate><title>Loss of Autoantibody Activity by Alteration in Autoantigen</title><author>Spitzer, Roger E. ; Stitzel, Ann E.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c399t-9cddb08b000099ebe36ec0e77900b37d4bc0969e8a00990f588abb5ffb1b94863</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1996</creationdate><topic>Adult</topic><topic>Antigen-Antibody Reactions - drug effects</topic><topic>Autoantibodies - blood</topic><topic>Autoantibodies - metabolism</topic><topic>Autoantibodies - pharmacology</topic><topic>Autoantigens - blood</topic><topic>Autoantigens - immunology</topic><topic>Autoantigens - metabolism</topic><topic>Biological and medical sciences</topic><topic>Complement C3 - metabolism</topic><topic>Complement C3 Nephritic Factor - metabolism</topic><topic>Complement C3 Nephritic Factor - pharmacology</topic><topic>Complement Factor B - metabolism</topic><topic>Complement Factor B - pharmacology</topic><topic>Female</topic><topic>Glomerulonephritis</topic><topic>Glomerulonephritis, Membranoproliferative - immunology</topic><topic>Humans</topic><topic>Medical sciences</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Nephropathies. Renovascular diseases. Renal failure</topic><toplevel>online_resources</toplevel><creatorcontrib>Spitzer, Roger E.</creatorcontrib><creatorcontrib>Stitzel, Ann E.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Clinical immunology and immunopathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Spitzer, Roger E.</au><au>Stitzel, Ann E.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Loss of Autoantibody Activity by Alteration in Autoantigen</atitle><jtitle>Clinical immunology and immunopathology</jtitle><addtitle>Clin Immunol Immunopathol</addtitle><date>1996-08-01</date><risdate>1996</risdate><volume>80</volume><issue>2</issue><spage>211</spage><epage>213</epage><pages>211-213</pages><issn>0090-1229</issn><eissn>1090-2341</eissn><coden>CLIIAT</coden><abstract>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.</abstract><cop>San Diego, CA</cop><cop>New York, NY</cop><cop>Boston</cop><pub>Elsevier Inc</pub><pmid>8764567</pmid><doi>10.1006/clin.1996.0116</doi><tpages>3</tpages></addata></record> |
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| identifier | ISSN: 0090-1229 |
| ispartof | Clinical immunology and immunopathology, 1996-08, Vol.80 (2), p.211-213 |
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| language | eng |
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| source | MEDLINE; Alma/SFX Local Collection |
| 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 |
| title | Loss of Autoantibody Activity by Alteration in Autoantigen |
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