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Adoptive transfer of allotype-specific suppressor cells inhibits thymus- independent immunoglobulin production in syngeneic athymic mice
(SJL X BALB)F1 suppressed mice have, in their lymphoid tissues, a population of suppressor T cells directed specifically against a paternal gamma G2a allotype (Ig-1b). Spleen or lymph node cells from these mice were injected into syngeneic nude mice and the effect on thymus-independent synthesis of...
Formato: | Texto |
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Lenguaje: | English |
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The Rockefeller University Press
1978
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2184955/ https://www.ncbi.nlm.nih.gov/pubmed/308982 |
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collection | PubMed |
description | (SJL X BALB)F1 suppressed mice have, in their lymphoid tissues, a population of suppressor T cells directed specifically against a paternal gamma G2a allotype (Ig-1b). Spleen or lymph node cells from these mice were injected into syngeneic nude mice and the effect on thymus-independent synthesis of Ig-1b in the athymic recipients was determined. After the injection of suppressor cells, Ig-1b disappeared from the serum of the recipients in a time course similar to that seen in normal mice. These results indicate that suppression occurs in the absence of thymus-derived helper cells, and they suggest that Ig-1b- producing B cells are the target of allotype-suppressor cells. |
format | Text |
id | pubmed-2184955 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1978 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-21849552008-04-17 Adoptive transfer of allotype-specific suppressor cells inhibits thymus- independent immunoglobulin production in syngeneic athymic mice J Exp Med Articles (SJL X BALB)F1 suppressed mice have, in their lymphoid tissues, a population of suppressor T cells directed specifically against a paternal gamma G2a allotype (Ig-1b). Spleen or lymph node cells from these mice were injected into syngeneic nude mice and the effect on thymus-independent synthesis of Ig-1b in the athymic recipients was determined. After the injection of suppressor cells, Ig-1b disappeared from the serum of the recipients in a time course similar to that seen in normal mice. These results indicate that suppression occurs in the absence of thymus-derived helper cells, and they suggest that Ig-1b- producing B cells are the target of allotype-suppressor cells. The Rockefeller University Press 1978-08-01 /pmc/articles/PMC2184955/ /pubmed/308982 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 Adoptive transfer of allotype-specific suppressor cells inhibits thymus- independent immunoglobulin production in syngeneic athymic mice |
title | Adoptive transfer of allotype-specific suppressor cells inhibits thymus- independent immunoglobulin production in syngeneic athymic mice |
title_full | Adoptive transfer of allotype-specific suppressor cells inhibits thymus- independent immunoglobulin production in syngeneic athymic mice |
title_fullStr | Adoptive transfer of allotype-specific suppressor cells inhibits thymus- independent immunoglobulin production in syngeneic athymic mice |
title_full_unstemmed | Adoptive transfer of allotype-specific suppressor cells inhibits thymus- independent immunoglobulin production in syngeneic athymic mice |
title_short | Adoptive transfer of allotype-specific suppressor cells inhibits thymus- independent immunoglobulin production in syngeneic athymic mice |
title_sort | adoptive transfer of allotype-specific suppressor cells inhibits thymus- independent immunoglobulin production in syngeneic athymic mice |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2184955/ https://www.ncbi.nlm.nih.gov/pubmed/308982 |