A transforming growth factor beta-like immunosuppressive factor in immunoglobulin G-binding factor

Immunoglobulin G-binding factors (IgG-BF), which are produced by cells of the immune system, inhibit antibody production. In this paper, we show that transforming growth factor-beta (TGF-beta) suppresses secondary in vitro anti-sheep red blood cell responses of mouse splenocytes and lipopolysacchari...

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Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 1995
Materias:
Articles
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2192234/
https://www.ncbi.nlm.nih.gov/pubmed/7500016
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collection PubMed
description Immunoglobulin G-binding factors (IgG-BF), which are produced by cells of the immune system, inhibit antibody production. In this paper, we show that transforming growth factor-beta (TGF-beta) suppresses secondary in vitro anti-sheep red blood cell responses of mouse splenocytes and lipopolysaccharide- or anti-IgM-stimulated mouse B cell responses in a way similar to, and with the same kinetics as, rodent IgG-BF. Moreover, the immunosuppressive activity of IgG-BF was totally neutralized by polyclonal and monoclonal anti-TGF-beta antibodies and it eluted with TGF-beta by gel exclusion chromatography, suggesting that a TGF-beta-like immunosuppressive factor is present in IgG-BF. We also show that TGF-beta behaves as an IgG-BF since it binds to insolubilized IgG, but not to insolubilized F(ab')2 or bovine serum albumin. Altogether, the data support the concept of a biological role for TGF-beta in the IgG-mediated negative feedback of antibody responses.
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spelling pubmed-21922342008-04-16 A transforming growth factor beta-like immunosuppressive factor in immunoglobulin G-binding factor J Exp Med Articles Immunoglobulin G-binding factors (IgG-BF), which are produced by cells of the immune system, inhibit antibody production. In this paper, we show that transforming growth factor-beta (TGF-beta) suppresses secondary in vitro anti-sheep red blood cell responses of mouse splenocytes and lipopolysaccharide- or anti-IgM-stimulated mouse B cell responses in a way similar to, and with the same kinetics as, rodent IgG-BF. Moreover, the immunosuppressive activity of IgG-BF was totally neutralized by polyclonal and monoclonal anti-TGF-beta antibodies and it eluted with TGF-beta by gel exclusion chromatography, suggesting that a TGF-beta-like immunosuppressive factor is present in IgG-BF. We also show that TGF-beta behaves as an IgG-BF since it binds to insolubilized IgG, but not to insolubilized F(ab')2 or bovine serum albumin. Altogether, the data support the concept of a biological role for TGF-beta in the IgG-mediated negative feedback of antibody responses. The Rockefeller University Press 1995-12-01 /pmc/articles/PMC2192234/ /pubmed/7500016 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
A transforming growth factor beta-like immunosuppressive factor in immunoglobulin G-binding factor
title A transforming growth factor beta-like immunosuppressive factor in immunoglobulin G-binding factor
title_full A transforming growth factor beta-like immunosuppressive factor in immunoglobulin G-binding factor
title_fullStr A transforming growth factor beta-like immunosuppressive factor in immunoglobulin G-binding factor
title_full_unstemmed A transforming growth factor beta-like immunosuppressive factor in immunoglobulin G-binding factor
title_short A transforming growth factor beta-like immunosuppressive factor in immunoglobulin G-binding factor
title_sort transforming growth factor beta-like immunosuppressive factor in immunoglobulin g-binding factor
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2192234/
https://www.ncbi.nlm.nih.gov/pubmed/7500016

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