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TWO KINDS OF ANTIGEN SUPPRESSION IN TUMOR CELLS REVEALED BY CELL FUSION
The Ehrlich ascites tumor, which has been subjected to prolonged selection for growth in allogeneic hosts, possesses powerful mechanisms for the suppression of antigens normally found on the cell surface. It has previously been shown (1, 2) that when cells in which surface antigens are fully express...
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Formato: | Texto |
Lenguaje: | English |
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The Rockefeller University Press
1972
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2139157/ https://www.ncbi.nlm.nih.gov/pubmed/5018053 |
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author | Klein, George Friberg, Sten Harris, Henry |
author_facet | Klein, George Friberg, Sten Harris, Henry |
author_sort | Klein, George |
collection | PubMed |
description | The Ehrlich ascites tumor, which has been subjected to prolonged selection for growth in allogeneic hosts, possesses powerful mechanisms for the suppression of antigens normally found on the cell surface. It has previously been shown (1, 2) that when cells in which surface antigens are fully expressed are fused with Ehrlich cells, the suppressive mechanisms of the latter continue to operate and the new surface antigens introduced into the hybrid cell by the other partner are also suppressed. In the present paper we describe the properties of hybrids in which one parent cell was the TA3 ascites carcinoma. There are two sublines of this carcinoma which originally arose as a spontaneous mammary carcinoma in a strain A mouse. The TA3/St line has a high concentration of H-2(a) antigens and shows a strain-specific transplantation behavior; the TA3/Ha subline has a drastically reduced antigen concentration and readily transgresses histoincompatibility barriers. The immunoresistant TA3/Ha subline arose spontaneously without having been subjected to any known immunological selection pressure. Hybridization of TA3/Ha cells with normal diploid ACA fibroblasts reestablished full expression of H-2(a) antigens in nine independently derived hybrid clones. Full reestablishment of both D- and K-end components of the H-2(a) complex could be demonstrated. In some hybrid clones the concentration of H-2(a) antigens was found to be comparable to that seen in (A x ACA)F(1) fibroblasts, whereas in others a higher concentration was observed, even exceeding, in some cases, the levels found in the TA3/St line. The H-2(f) complex, contributed by the ACA parent cell, was fully expressed in eight of the nine hybrid clones studied. Antigen suppression thus behaves as a recessive character in the TA3/Ha hybrids, whereas in the Ehrlich hybrids antigen suppression is dominant. |
format | Text |
id | pubmed-2139157 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1972 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-21391572008-04-17 TWO KINDS OF ANTIGEN SUPPRESSION IN TUMOR CELLS REVEALED BY CELL FUSION Klein, George Friberg, Sten Harris, Henry J Exp Med Article The Ehrlich ascites tumor, which has been subjected to prolonged selection for growth in allogeneic hosts, possesses powerful mechanisms for the suppression of antigens normally found on the cell surface. It has previously been shown (1, 2) that when cells in which surface antigens are fully expressed are fused with Ehrlich cells, the suppressive mechanisms of the latter continue to operate and the new surface antigens introduced into the hybrid cell by the other partner are also suppressed. In the present paper we describe the properties of hybrids in which one parent cell was the TA3 ascites carcinoma. There are two sublines of this carcinoma which originally arose as a spontaneous mammary carcinoma in a strain A mouse. The TA3/St line has a high concentration of H-2(a) antigens and shows a strain-specific transplantation behavior; the TA3/Ha subline has a drastically reduced antigen concentration and readily transgresses histoincompatibility barriers. The immunoresistant TA3/Ha subline arose spontaneously without having been subjected to any known immunological selection pressure. Hybridization of TA3/Ha cells with normal diploid ACA fibroblasts reestablished full expression of H-2(a) antigens in nine independently derived hybrid clones. Full reestablishment of both D- and K-end components of the H-2(a) complex could be demonstrated. In some hybrid clones the concentration of H-2(a) antigens was found to be comparable to that seen in (A x ACA)F(1) fibroblasts, whereas in others a higher concentration was observed, even exceeding, in some cases, the levels found in the TA3/St line. The H-2(f) complex, contributed by the ACA parent cell, was fully expressed in eight of the nine hybrid clones studied. Antigen suppression thus behaves as a recessive character in the TA3/Ha hybrids, whereas in the Ehrlich hybrids antigen suppression is dominant. The Rockefeller University Press 1972-03-31 /pmc/articles/PMC2139157/ /pubmed/5018053 Text en Copyright © 1972 by The Rockefeller University Press 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 | Article Klein, George Friberg, Sten Harris, Henry TWO KINDS OF ANTIGEN SUPPRESSION IN TUMOR CELLS REVEALED BY CELL FUSION |
title | TWO KINDS OF ANTIGEN SUPPRESSION IN TUMOR CELLS REVEALED BY CELL FUSION |
title_full | TWO KINDS OF ANTIGEN SUPPRESSION IN TUMOR CELLS REVEALED BY CELL FUSION |
title_fullStr | TWO KINDS OF ANTIGEN SUPPRESSION IN TUMOR CELLS REVEALED BY CELL FUSION |
title_full_unstemmed | TWO KINDS OF ANTIGEN SUPPRESSION IN TUMOR CELLS REVEALED BY CELL FUSION |
title_short | TWO KINDS OF ANTIGEN SUPPRESSION IN TUMOR CELLS REVEALED BY CELL FUSION |
title_sort | two kinds of antigen suppression in tumor cells revealed by cell fusion |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2139157/ https://www.ncbi.nlm.nih.gov/pubmed/5018053 |
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