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Role of the major histocompatibility gene products in regulating the antibody response to dinitrophenylated poly(L-Glu55,L-Ala35,L-Phe9)n
These studies were carried out to investigate the potential helper T cell repertoire specific for the random copolymer poly(L-Glu55,L-Ala35, L-Phe9)n(GL phi 9) of responder, nonresponder, and (responder x nonresponder)F1 murine strains. We tested the ability of these T cells to collaborate with dini...
Formato: | Texto |
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Lenguaje: | English |
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The Rockefeller University Press
1980
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2185948/ https://www.ncbi.nlm.nih.gov/pubmed/6156986 |
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collection | PubMed |
description | These studies were carried out to investigate the potential helper T cell repertoire specific for the random copolymer poly(L-Glu55,L-Ala35, L-Phe9)n(GL phi 9) of responder, nonresponder, and (responder x nonresponder)F1 murine strains. We tested the ability of these T cells to collaborate with dinitrophenyl (DNP)-specific primary and secondary B lymphocytes of each strain in response to the antigen CNP-GL phi 9 in the splenic-fragment culture system. The results of these experiments show that there are GL phi 9-specific T lymphocytes in the responder, nonresponder, and F1 strains; but that these three GL phi 9-specific T cell populations differ in their collaborative potential. Responder T cells are able to collaborate with their own syngeneic responder B cells as well as the allogeneic nonresponder B cells in a syngeneic fashion. The F1 T cell population resembles that of the nonresponder in its ability to collaborate with only responder B cells in a syngeneic fashion. Analysis carried out using appropriately selected mouse strains indicate that these results are unlikely to be a result of positive or negative allogeneic effects. The results obtained suggest that individuals within a given murine strain do possess the capacity to collaborate in a syngeneic fashion with B cells of any other MHC- allogeneic strain as well as their own MHC-identical B cells. The nonresponder status in the response to GL phi 9 appears to be the result of a deletion of T cells capable of recognizing antigen in the context of B cells of the nonresponder haplotype. Thus, the MHC gene products appear to play a determinative role in shaping the expressed helper T cell specificity repertoire within an individual mouse strain. |
format | Text |
id | pubmed-2185948 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1980 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-21859482008-04-17 Role of the major histocompatibility gene products in regulating the antibody response to dinitrophenylated poly(L-Glu55,L-Ala35,L-Phe9)n J Exp Med Articles These studies were carried out to investigate the potential helper T cell repertoire specific for the random copolymer poly(L-Glu55,L-Ala35, L-Phe9)n(GL phi 9) of responder, nonresponder, and (responder x nonresponder)F1 murine strains. We tested the ability of these T cells to collaborate with dinitrophenyl (DNP)-specific primary and secondary B lymphocytes of each strain in response to the antigen CNP-GL phi 9 in the splenic-fragment culture system. The results of these experiments show that there are GL phi 9-specific T lymphocytes in the responder, nonresponder, and F1 strains; but that these three GL phi 9-specific T cell populations differ in their collaborative potential. Responder T cells are able to collaborate with their own syngeneic responder B cells as well as the allogeneic nonresponder B cells in a syngeneic fashion. The F1 T cell population resembles that of the nonresponder in its ability to collaborate with only responder B cells in a syngeneic fashion. Analysis carried out using appropriately selected mouse strains indicate that these results are unlikely to be a result of positive or negative allogeneic effects. The results obtained suggest that individuals within a given murine strain do possess the capacity to collaborate in a syngeneic fashion with B cells of any other MHC- allogeneic strain as well as their own MHC-identical B cells. The nonresponder status in the response to GL phi 9 appears to be the result of a deletion of T cells capable of recognizing antigen in the context of B cells of the nonresponder haplotype. Thus, the MHC gene products appear to play a determinative role in shaping the expressed helper T cell specificity repertoire within an individual mouse strain. The Rockefeller University Press 1980-08-01 /pmc/articles/PMC2185948/ /pubmed/6156986 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 Role of the major histocompatibility gene products in regulating the antibody response to dinitrophenylated poly(L-Glu55,L-Ala35,L-Phe9)n |
title | Role of the major histocompatibility gene products in regulating the antibody response to dinitrophenylated poly(L-Glu55,L-Ala35,L-Phe9)n |
title_full | Role of the major histocompatibility gene products in regulating the antibody response to dinitrophenylated poly(L-Glu55,L-Ala35,L-Phe9)n |
title_fullStr | Role of the major histocompatibility gene products in regulating the antibody response to dinitrophenylated poly(L-Glu55,L-Ala35,L-Phe9)n |
title_full_unstemmed | Role of the major histocompatibility gene products in regulating the antibody response to dinitrophenylated poly(L-Glu55,L-Ala35,L-Phe9)n |
title_short | Role of the major histocompatibility gene products in regulating the antibody response to dinitrophenylated poly(L-Glu55,L-Ala35,L-Phe9)n |
title_sort | role of the major histocompatibility gene products in regulating the antibody response to dinitrophenylated poly(l-glu55,l-ala35,l-phe9)n |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2185948/ https://www.ncbi.nlm.nih.gov/pubmed/6156986 |