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Treatment of (NZB x NZW)F1 disease with anti-I-A monoclonal antibodies
(NZB x NZW)F1 mice spontaneously develop an autoimmune syndrome characterized by a fatal immune complex glomerulonephritis. Administration of monoclonal antibodies specific for an I region gene product (I-Az) of the H-2 haplotype associated with susceptibility to glomerulonephritis in these animals...
Formato: | Texto |
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Lenguaje: | English |
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The Rockefeller University Press
1983
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2187363/ https://www.ncbi.nlm.nih.gov/pubmed/6578293 |
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collection | PubMed |
description | (NZB x NZW)F1 mice spontaneously develop an autoimmune syndrome characterized by a fatal immune complex glomerulonephritis. Administration of monoclonal antibodies specific for an I region gene product (I-Az) of the H-2 haplotype associated with susceptibility to glomerulonephritis in these animals produced a remission in female mice with established renal disease. The results demonstrated that anti-I-A therapy stabilized the level of proteinuria and increased the 1-yr survival rate from 10% to greater than 90% in treated animals relative to control mice. These findings may ultimately have therapeutic potential for the treatment of systemic lupus erythematosus. |
format | Text |
id | pubmed-2187363 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1983 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-21873632008-04-17 Treatment of (NZB x NZW)F1 disease with anti-I-A monoclonal antibodies J Exp Med Articles (NZB x NZW)F1 mice spontaneously develop an autoimmune syndrome characterized by a fatal immune complex glomerulonephritis. Administration of monoclonal antibodies specific for an I region gene product (I-Az) of the H-2 haplotype associated with susceptibility to glomerulonephritis in these animals produced a remission in female mice with established renal disease. The results demonstrated that anti-I-A therapy stabilized the level of proteinuria and increased the 1-yr survival rate from 10% to greater than 90% in treated animals relative to control mice. These findings may ultimately have therapeutic potential for the treatment of systemic lupus erythematosus. The Rockefeller University Press 1983-10-01 /pmc/articles/PMC2187363/ /pubmed/6578293 Text en This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/). |
spellingShingle | Articles Treatment of (NZB x NZW)F1 disease with anti-I-A monoclonal antibodies |
title | Treatment of (NZB x NZW)F1 disease with anti-I-A monoclonal antibodies |
title_full | Treatment of (NZB x NZW)F1 disease with anti-I-A monoclonal antibodies |
title_fullStr | Treatment of (NZB x NZW)F1 disease with anti-I-A monoclonal antibodies |
title_full_unstemmed | Treatment of (NZB x NZW)F1 disease with anti-I-A monoclonal antibodies |
title_short | Treatment of (NZB x NZW)F1 disease with anti-I-A monoclonal antibodies |
title_sort | treatment of (nzb x nzw)f1 disease with anti-i-a monoclonal antibodies |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2187363/ https://www.ncbi.nlm.nih.gov/pubmed/6578293 |