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Mechanism responsible for the induction of I-J restriction on TS3 suppressor cells

The mechanisms responsible for the induction of I-J restrictions on third-order suppressor T cells (TS3) were analyzed. The I-J phenotype of the antigen-coupled cells used for priming restricted the specificity of the TS3 population. Thus, TS3 cells were only generated after priming with antigen-cou...

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Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 1982
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2186842/
https://www.ncbi.nlm.nih.gov/pubmed/6215458
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description The mechanisms responsible for the induction of I-J restrictions on third-order suppressor T cells (TS3) were analyzed. The I-J phenotype of the antigen-coupled cells used for priming restricted the specificity of the TS3 population. Thus, TS3 cells were only generated after priming with antigen-coupled I-J homologous cells. Identity at the I-JM (and I-E) subregions was sufficient for TS3 induction. Furthermore, priming of H-2 heterozygous mice with antigen-coupled parental cells generated TS3 that were restricted to the parental haplotype used for priming. The splenic cell population responsible for antigen presentation and induction of TS3 cells was fractionated. The cells involved in antigen presentation were found in the splenic adherent population and were absent in the fraction containing splenic nonadherent T and B cells. The subsequent activation and interaction of TS3 cells is also restricted by genes in the H-2 complex. The results are discussed in terms of a general mechanism responsible for the induction of restrictions in T helper and TS3 cells.
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spelling pubmed-21868422008-04-17 Mechanism responsible for the induction of I-J restriction on TS3 suppressor cells J Exp Med Articles The mechanisms responsible for the induction of I-J restrictions on third-order suppressor T cells (TS3) were analyzed. The I-J phenotype of the antigen-coupled cells used for priming restricted the specificity of the TS3 population. Thus, TS3 cells were only generated after priming with antigen-coupled I-J homologous cells. Identity at the I-JM (and I-E) subregions was sufficient for TS3 induction. Furthermore, priming of H-2 heterozygous mice with antigen-coupled parental cells generated TS3 that were restricted to the parental haplotype used for priming. The splenic cell population responsible for antigen presentation and induction of TS3 cells was fractionated. The cells involved in antigen presentation were found in the splenic adherent population and were absent in the fraction containing splenic nonadherent T and B cells. The subsequent activation and interaction of TS3 cells is also restricted by genes in the H-2 complex. The results are discussed in terms of a general mechanism responsible for the induction of restrictions in T helper and TS3 cells. The Rockefeller University Press 1982-11-01 /pmc/articles/PMC2186842/ /pubmed/6215458 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
Mechanism responsible for the induction of I-J restriction on TS3 suppressor cells
title Mechanism responsible for the induction of I-J restriction on TS3 suppressor cells
title_full Mechanism responsible for the induction of I-J restriction on TS3 suppressor cells
title_fullStr Mechanism responsible for the induction of I-J restriction on TS3 suppressor cells
title_full_unstemmed Mechanism responsible for the induction of I-J restriction on TS3 suppressor cells
title_short Mechanism responsible for the induction of I-J restriction on TS3 suppressor cells
title_sort mechanism responsible for the induction of i-j restriction on ts3 suppressor cells
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2186842/
https://www.ncbi.nlm.nih.gov/pubmed/6215458