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Anti-idiotype induced regulation of helper cell function for the response to phosphorylcholine in adult BALB/c mice

An adoptive secondary antibody response to phosphorylcholine (PC) can be generated by the transfer of keyhole limpet hemocyanin (KLH)-primed T cells, PC-bovine gamma globulin-primed B cells, and PC-KLH into irradiated syngeneic BALB/c mice. If the KLH-primed T-cell donors were pretreated with anti-i...

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Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 1978
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2185045/
https://www.ncbi.nlm.nih.gov/pubmed/309912
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description An adoptive secondary antibody response to phosphorylcholine (PC) can be generated by the transfer of keyhole limpet hemocyanin (KLH)-primed T cells, PC-bovine gamma globulin-primed B cells, and PC-KLH into irradiated syngeneic BALB/c mice. If the KLH-primed T-cell donors were pretreated with anti-idiotype antibodies directed against the BALB/c PC- binding myeloma TEPC 15, their T cells were unable to collaborate effectively with PC-primed B cells; moreover, they could suppress the helper activity of T cells from normal mice for the PC-KLH response. The Ly phenotype of these T cells was found to be Ly 1-, 2+. The specificity of the suppressor T-cell population induced by anti-T15 treatment appears to be both for idiotype (hapten) and carrier, since the suppressor T cells fail to interfere with the antibody response to PC on a heterologous carrier, nor do they suppress the response to trinitrophenol-KLH.
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spelling pubmed-21850452008-04-17 Anti-idiotype induced regulation of helper cell function for the response to phosphorylcholine in adult BALB/c mice J Exp Med Articles An adoptive secondary antibody response to phosphorylcholine (PC) can be generated by the transfer of keyhole limpet hemocyanin (KLH)-primed T cells, PC-bovine gamma globulin-primed B cells, and PC-KLH into irradiated syngeneic BALB/c mice. If the KLH-primed T-cell donors were pretreated with anti-idiotype antibodies directed against the BALB/c PC- binding myeloma TEPC 15, their T cells were unable to collaborate effectively with PC-primed B cells; moreover, they could suppress the helper activity of T cells from normal mice for the PC-KLH response. The Ly phenotype of these T cells was found to be Ly 1-, 2+. The specificity of the suppressor T-cell population induced by anti-T15 treatment appears to be both for idiotype (hapten) and carrier, since the suppressor T cells fail to interfere with the antibody response to PC on a heterologous carrier, nor do they suppress the response to trinitrophenol-KLH. The Rockefeller University Press 1978-11-01 /pmc/articles/PMC2185045/ /pubmed/309912 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
Anti-idiotype induced regulation of helper cell function for the response to phosphorylcholine in adult BALB/c mice
title Anti-idiotype induced regulation of helper cell function for the response to phosphorylcholine in adult BALB/c mice
title_full Anti-idiotype induced regulation of helper cell function for the response to phosphorylcholine in adult BALB/c mice
title_fullStr Anti-idiotype induced regulation of helper cell function for the response to phosphorylcholine in adult BALB/c mice
title_full_unstemmed Anti-idiotype induced regulation of helper cell function for the response to phosphorylcholine in adult BALB/c mice
title_short Anti-idiotype induced regulation of helper cell function for the response to phosphorylcholine in adult BALB/c mice
title_sort anti-idiotype induced regulation of helper cell function for the response to phosphorylcholine in adult balb/c mice
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2185045/
https://www.ncbi.nlm.nih.gov/pubmed/309912