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A regulatory role for the memory B cell as suppressor-inducer of feedback control

A regulatory role is proposed for the antigen-responsive B cell, as suppressor-inducer of feedback control during the secondary response in vivo. In a double adoptive transfer of memory cells primed to a thymus- dependent antigen from one irradiated host to another, antigen-specific suppressors are...

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Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 1983
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2186930/
https://www.ncbi.nlm.nih.gov/pubmed/6185613
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description A regulatory role is proposed for the antigen-responsive B cell, as suppressor-inducer of feedback control during the secondary response in vivo. In a double adoptive transfer of memory cells primed to a thymus- dependent antigen from one irradiated host to another, antigen-specific suppressors are generated after a critical time in the primary recipient, able to entirely ablate a secondary anti-hapten response. Positive cell selection in the fluorescence-activated cell sorter confirmed that suppression was mediated by an Lyt-2+ T cell; however, positively selected B cells were also inhibitory and able to induce suppressors in a carrier-specific manner: Bhapten induced suppressors in a carrier-primed population, and Bcarrier induced suppressors in a hapten-carrier population. At the peak of the antibody response in the primary host, memory B cells and their progeny were unable to differentiate further to plasma cells due to their intrinsic suppressor- inducer activity, but this autoregulatory circuit could be severed by adoptive transfer to carrier-primed, X-irradiated recipients.
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spelling pubmed-21869302008-04-17 A regulatory role for the memory B cell as suppressor-inducer of feedback control J Exp Med Articles A regulatory role is proposed for the antigen-responsive B cell, as suppressor-inducer of feedback control during the secondary response in vivo. In a double adoptive transfer of memory cells primed to a thymus- dependent antigen from one irradiated host to another, antigen-specific suppressors are generated after a critical time in the primary recipient, able to entirely ablate a secondary anti-hapten response. Positive cell selection in the fluorescence-activated cell sorter confirmed that suppression was mediated by an Lyt-2+ T cell; however, positively selected B cells were also inhibitory and able to induce suppressors in a carrier-specific manner: Bhapten induced suppressors in a carrier-primed population, and Bcarrier induced suppressors in a hapten-carrier population. At the peak of the antibody response in the primary host, memory B cells and their progeny were unable to differentiate further to plasma cells due to their intrinsic suppressor- inducer activity, but this autoregulatory circuit could be severed by adoptive transfer to carrier-primed, X-irradiated recipients. The Rockefeller University Press 1983-02-01 /pmc/articles/PMC2186930/ /pubmed/6185613 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 regulatory role for the memory B cell as suppressor-inducer of feedback control
title A regulatory role for the memory B cell as suppressor-inducer of feedback control
title_full A regulatory role for the memory B cell as suppressor-inducer of feedback control
title_fullStr A regulatory role for the memory B cell as suppressor-inducer of feedback control
title_full_unstemmed A regulatory role for the memory B cell as suppressor-inducer of feedback control
title_short A regulatory role for the memory B cell as suppressor-inducer of feedback control
title_sort regulatory role for the memory b cell as suppressor-inducer of feedback control
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2186930/
https://www.ncbi.nlm.nih.gov/pubmed/6185613