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Tolerance for self IG at the level of the Ly1+ T cell
Experiments presented in this report demonstrate that specificity of the Ly1+ T cell proliferative response to NP-modified Ig is controlled by Igh-C-linked genes. In addition, we describe the mechanism whereby Igh-C-encoded molecules influence Ly1+ T cell activity. We show that Igh-C-linked control...
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/PMC2187155/ https://www.ncbi.nlm.nih.gov/pubmed/6417259 |
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collection | PubMed |
description | Experiments presented in this report demonstrate that specificity of the Ly1+ T cell proliferative response to NP-modified Ig is controlled by Igh-C-linked genes. In addition, we describe the mechanism whereby Igh-C-encoded molecules influence Ly1+ T cell activity. We show that Igh-C-linked control of T cell responses to NP-modified Ig is a secondary consequence of naturally acquired tolerance for self Ig. Unresponsiveness to self Ig is not due to a defect expressed functionally at the level of the antigen-presenting cell, nor is it associated with active suppression. These results suggest that tolerance for self Ig at the level of the Ly1+ T cell is due to functional deletion of Ly1+ T cell clones specific for self Ig. The possibility is considered that regulatory effects mediated by passively administered antibodies may in part be due to induction of Ly1+ T cell tolerance for self Ig. |
format | Text |
id | pubmed-2187155 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1983 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-21871552008-04-17 Tolerance for self IG at the level of the Ly1+ T cell J Exp Med Articles Experiments presented in this report demonstrate that specificity of the Ly1+ T cell proliferative response to NP-modified Ig is controlled by Igh-C-linked genes. In addition, we describe the mechanism whereby Igh-C-encoded molecules influence Ly1+ T cell activity. We show that Igh-C-linked control of T cell responses to NP-modified Ig is a secondary consequence of naturally acquired tolerance for self Ig. Unresponsiveness to self Ig is not due to a defect expressed functionally at the level of the antigen-presenting cell, nor is it associated with active suppression. These results suggest that tolerance for self Ig at the level of the Ly1+ T cell is due to functional deletion of Ly1+ T cell clones specific for self Ig. The possibility is considered that regulatory effects mediated by passively administered antibodies may in part be due to induction of Ly1+ T cell tolerance for self Ig. The Rockefeller University Press 1983-12-01 /pmc/articles/PMC2187155/ /pubmed/6417259 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 Tolerance for self IG at the level of the Ly1+ T cell |
title | Tolerance for self IG at the level of the Ly1+ T cell |
title_full | Tolerance for self IG at the level of the Ly1+ T cell |
title_fullStr | Tolerance for self IG at the level of the Ly1+ T cell |
title_full_unstemmed | Tolerance for self IG at the level of the Ly1+ T cell |
title_short | Tolerance for self IG at the level of the Ly1+ T cell |
title_sort | tolerance for self ig at the level of the ly1+ t cell |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2187155/ https://www.ncbi.nlm.nih.gov/pubmed/6417259 |