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Distinct Ir genes for helper and killer cells in the cytotoxic response to H-Y antigen

The H-Y-specific cytotoxic T-cell response requires helper cells: cells from bone marrow chimeras B6 X CBA leads to B6, B6 X CBA leads to B10.A (5R), or B6 X CBA leads to CBA are each unable to respond to H-2k male cells. If, however, cells from B6 X CBA leads to B6 or B6 X CBA leads to B10.A (5R) c...

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Detalles Bibliográficos
Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 1979
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2185706/
https://www.ncbi.nlm.nih.gov/pubmed/115957
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collection PubMed
description The H-Y-specific cytotoxic T-cell response requires helper cells: cells from bone marrow chimeras B6 X CBA leads to B6, B6 X CBA leads to B10.A (5R), or B6 X CBA leads to CBA are each unable to respond to H-2k male cells. If, however, cells from B6 X CBA leads to B6 or B6 X CBA leads to B10.A (5R) chimeras are adoptively transferred together with cells from B6 X CBA leads to CBA chimeras, H-Y-specific CTL restricted to H- 2k can be obtained. Thus, cells from B6 X CBA leads to B6 or B6 X CBA leads to B10.,A (5R) chimeras (restricted to the left end of the H-2b haplotype) can help CTL precursors from B6 X CBA leads to CBA chimeras (restricted to H-2k). The two classes of T cells required for the CTL response to H-Y antigen are controlled by different IR genes. All H-Y- specific CTL obtained from chimeras B6 + CBA leads to B6 X CBA were found to be of B6 origin. This suggests that CTL or their precursors must express antigens encoded in the left end of the H-2b haplotype for interaction with helper cells.
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spelling pubmed-21857062008-04-17 Distinct Ir genes for helper and killer cells in the cytotoxic response to H-Y antigen J Exp Med Articles The H-Y-specific cytotoxic T-cell response requires helper cells: cells from bone marrow chimeras B6 X CBA leads to B6, B6 X CBA leads to B10.A (5R), or B6 X CBA leads to CBA are each unable to respond to H-2k male cells. If, however, cells from B6 X CBA leads to B6 or B6 X CBA leads to B10.A (5R) chimeras are adoptively transferred together with cells from B6 X CBA leads to CBA chimeras, H-Y-specific CTL restricted to H- 2k can be obtained. Thus, cells from B6 X CBA leads to B6 or B6 X CBA leads to B10.,A (5R) chimeras (restricted to the left end of the H-2b haplotype) can help CTL precursors from B6 X CBA leads to CBA chimeras (restricted to H-2k). The two classes of T cells required for the CTL response to H-Y antigen are controlled by different IR genes. All H-Y- specific CTL obtained from chimeras B6 + CBA leads to B6 X CBA were found to be of B6 origin. This suggests that CTL or their precursors must express antigens encoded in the left end of the H-2b haplotype for interaction with helper cells. The Rockefeller University Press 1979-11-01 /pmc/articles/PMC2185706/ /pubmed/115957 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
Distinct Ir genes for helper and killer cells in the cytotoxic response to H-Y antigen
title Distinct Ir genes for helper and killer cells in the cytotoxic response to H-Y antigen
title_full Distinct Ir genes for helper and killer cells in the cytotoxic response to H-Y antigen
title_fullStr Distinct Ir genes for helper and killer cells in the cytotoxic response to H-Y antigen
title_full_unstemmed Distinct Ir genes for helper and killer cells in the cytotoxic response to H-Y antigen
title_short Distinct Ir genes for helper and killer cells in the cytotoxic response to H-Y antigen
title_sort distinct ir genes for helper and killer cells in the cytotoxic response to h-y antigen
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2185706/
https://www.ncbi.nlm.nih.gov/pubmed/115957