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Immune complexes can trigger specific, T cell-dependent, autoanti-IgG antibody production in mice
Immunization of mice with a combination of passively administered syngeneic IgG (anti-p-azophenylarsonate [anti-Ars]) antibody and a soluble, multivalent form of the antibody's corresponding antigen (Limulus polyphemus hemocyanin conjugated with Ars [Lph-Ars]) resulted in specific autoanti-IgG...
Formato: | Texto |
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Lenguaje: | English |
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The Rockefeller University Press
1985
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2187542/ https://www.ncbi.nlm.nih.gov/pubmed/2578542 |
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collection | PubMed |
description | Immunization of mice with a combination of passively administered syngeneic IgG (anti-p-azophenylarsonate [anti-Ars]) antibody and a soluble, multivalent form of the antibody's corresponding antigen (Limulus polyphemus hemocyanin conjugated with Ars [Lph-Ars]) resulted in specific autoanti-IgG Fc (rheumatoid factor) production. The response was rapid and only anti-IgG of the IgM isotype is found. Because immunization with either the IgG antibody or the antigen alone did not result in rheumatoid antibody production, immune complexes appear to be the active form of the immunogens. Antibody/antigen ratios that resulted in maximal anti-IgG antibody responses were the same as those required for peak in vitro immunoprecipitation, i.e., equivalence. Previous exposure of the mice to the exogenously supplied antigen was not required for the response. The response to immune complexes is specific because mice immunized with IgG2a-containing complexes produced autoanti-IgG2a, while mice immunized with IgG1- containing complexes produced anti-IgG1 with little reactivity to other IgG isotypes. IgG2a blocked in its complement-fixing capacity was more effective in eliciting the anti-IgG2a response than native IgG2a, suggesting a possible role for the complement system in modulating the anti-IgG2a response. Induction of rheumatoid factor production by immune complexes could be induced in xid mice but not in nu/nu mice, indicating T lymphocyte dependence of the response. In contrast, the B lymphocyte activator lipopolysaccharide was able to elicit vigorous rheumatoid factor production in both nu/nu and normal mice, demonstrating that nu/nu mice contain B cells capable of making the response. Rheumatoid antibody produced in the immune complex- or LPS- induced responses is Fc specific and has relatively low affinity for IgG that is not bound to antigen. |
format | Text |
id | pubmed-2187542 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1985 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-21875422008-04-17 Immune complexes can trigger specific, T cell-dependent, autoanti-IgG antibody production in mice J Exp Med Articles Immunization of mice with a combination of passively administered syngeneic IgG (anti-p-azophenylarsonate [anti-Ars]) antibody and a soluble, multivalent form of the antibody's corresponding antigen (Limulus polyphemus hemocyanin conjugated with Ars [Lph-Ars]) resulted in specific autoanti-IgG Fc (rheumatoid factor) production. The response was rapid and only anti-IgG of the IgM isotype is found. Because immunization with either the IgG antibody or the antigen alone did not result in rheumatoid antibody production, immune complexes appear to be the active form of the immunogens. Antibody/antigen ratios that resulted in maximal anti-IgG antibody responses were the same as those required for peak in vitro immunoprecipitation, i.e., equivalence. Previous exposure of the mice to the exogenously supplied antigen was not required for the response. The response to immune complexes is specific because mice immunized with IgG2a-containing complexes produced autoanti-IgG2a, while mice immunized with IgG1- containing complexes produced anti-IgG1 with little reactivity to other IgG isotypes. IgG2a blocked in its complement-fixing capacity was more effective in eliciting the anti-IgG2a response than native IgG2a, suggesting a possible role for the complement system in modulating the anti-IgG2a response. Induction of rheumatoid factor production by immune complexes could be induced in xid mice but not in nu/nu mice, indicating T lymphocyte dependence of the response. In contrast, the B lymphocyte activator lipopolysaccharide was able to elicit vigorous rheumatoid factor production in both nu/nu and normal mice, demonstrating that nu/nu mice contain B cells capable of making the response. Rheumatoid antibody produced in the immune complex- or LPS- induced responses is Fc specific and has relatively low affinity for IgG that is not bound to antigen. The Rockefeller University Press 1985-01-01 /pmc/articles/PMC2187542/ /pubmed/2578542 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 Immune complexes can trigger specific, T cell-dependent, autoanti-IgG antibody production in mice |
title | Immune complexes can trigger specific, T cell-dependent, autoanti-IgG antibody production in mice |
title_full | Immune complexes can trigger specific, T cell-dependent, autoanti-IgG antibody production in mice |
title_fullStr | Immune complexes can trigger specific, T cell-dependent, autoanti-IgG antibody production in mice |
title_full_unstemmed | Immune complexes can trigger specific, T cell-dependent, autoanti-IgG antibody production in mice |
title_short | Immune complexes can trigger specific, T cell-dependent, autoanti-IgG antibody production in mice |
title_sort | immune complexes can trigger specific, t cell-dependent, autoanti-igg antibody production in mice |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2187542/ https://www.ncbi.nlm.nih.gov/pubmed/2578542 |