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Antigenic properties of cultured tumor cell lines derived from spleens of Friend virus-infected BALB/c and BALB/c-H-2b mice
BALB/c-H-2b (BALB.B) mice are less susceptible to the Friend virus (FV) disease syndrome than congenic BALB/c (H-2d) mice, and spleen cells from FV-infected BALB.B mice are markedly less tumorigenic on transplantation to syngeneic hosts than those from FV-infected BALB/c mice. For these reasons we i...
Formato: | Texto |
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Lenguaje: | English |
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The Rockefeller University Press
1975
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2190061/ https://www.ncbi.nlm.nih.gov/pubmed/1194854 |
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collection | PubMed |
description | BALB/c-H-2b (BALB.B) mice are less susceptible to the Friend virus (FV) disease syndrome than congenic BALB/c (H-2d) mice, and spleen cells from FV-infected BALB.B mice are markedly less tumorigenic on transplantation to syngeneic hosts than those from FV-infected BALB/c mice. For these reasons we investigated the expression of FV-associated cell surface antigens on cultured, FV-trnasformed cell lines of BALB.B and BALB/c origin. Both cell lines induced transplantation immunity in syngeneic hosts toward further implantations of the same tumor, BALB.B cells being significantly more potent in this respect than BALB/c cells. BALB.B tumor cells, which produce complete, infectious FV, expressed both the cell surface antigen, FMR (corresponding to the cytotoxic antibodies in anti-FV antisera), and virus envelope antigen (VEA, corresponding to the virus-neutralizing antibodies in the anti-FV antisera). BALB/c tumor cells, on the other hand, which are FV- nonproducers, expressed no FMR antigen, but did express VEA on their surfaces for at least 100 passages in culture. These cells could induce FV-neutralizing but not cytotoxic anti-FMR antibodies when used to immunize syngeneic hosts. The absence of FMR antigen may be the basis for the reduced capacity of BALB/c tumor cells, by comparison with BALB.B tumor cells, to induce transplantation immunity. After about the 125th serial transfer in culture, BALB/c tumor cells spontaneously ceased to express VEA and simultaneously became very weak inducers of transplantation immunity in BALB/c hosts. This loss of VEA did not stem from the loss of either the spleen focus-forming virus or the helper virus genomes from these cells, since both viruses could still be recovered from the cell line. |
format | Text |
id | pubmed-2190061 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1975 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-21900612008-04-17 Antigenic properties of cultured tumor cell lines derived from spleens of Friend virus-infected BALB/c and BALB/c-H-2b mice J Exp Med Articles BALB/c-H-2b (BALB.B) mice are less susceptible to the Friend virus (FV) disease syndrome than congenic BALB/c (H-2d) mice, and spleen cells from FV-infected BALB.B mice are markedly less tumorigenic on transplantation to syngeneic hosts than those from FV-infected BALB/c mice. For these reasons we investigated the expression of FV-associated cell surface antigens on cultured, FV-trnasformed cell lines of BALB.B and BALB/c origin. Both cell lines induced transplantation immunity in syngeneic hosts toward further implantations of the same tumor, BALB.B cells being significantly more potent in this respect than BALB/c cells. BALB.B tumor cells, which produce complete, infectious FV, expressed both the cell surface antigen, FMR (corresponding to the cytotoxic antibodies in anti-FV antisera), and virus envelope antigen (VEA, corresponding to the virus-neutralizing antibodies in the anti-FV antisera). BALB/c tumor cells, on the other hand, which are FV- nonproducers, expressed no FMR antigen, but did express VEA on their surfaces for at least 100 passages in culture. These cells could induce FV-neutralizing but not cytotoxic anti-FMR antibodies when used to immunize syngeneic hosts. The absence of FMR antigen may be the basis for the reduced capacity of BALB/c tumor cells, by comparison with BALB.B tumor cells, to induce transplantation immunity. After about the 125th serial transfer in culture, BALB/c tumor cells spontaneously ceased to express VEA and simultaneously became very weak inducers of transplantation immunity in BALB/c hosts. This loss of VEA did not stem from the loss of either the spleen focus-forming virus or the helper virus genomes from these cells, since both viruses could still be recovered from the cell line. The Rockefeller University Press 1975-12-01 /pmc/articles/PMC2190061/ /pubmed/1194854 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 Antigenic properties of cultured tumor cell lines derived from spleens of Friend virus-infected BALB/c and BALB/c-H-2b mice |
title | Antigenic properties of cultured tumor cell lines derived from spleens of Friend virus-infected BALB/c and BALB/c-H-2b mice |
title_full | Antigenic properties of cultured tumor cell lines derived from spleens of Friend virus-infected BALB/c and BALB/c-H-2b mice |
title_fullStr | Antigenic properties of cultured tumor cell lines derived from spleens of Friend virus-infected BALB/c and BALB/c-H-2b mice |
title_full_unstemmed | Antigenic properties of cultured tumor cell lines derived from spleens of Friend virus-infected BALB/c and BALB/c-H-2b mice |
title_short | Antigenic properties of cultured tumor cell lines derived from spleens of Friend virus-infected BALB/c and BALB/c-H-2b mice |
title_sort | antigenic properties of cultured tumor cell lines derived from spleens of friend virus-infected balb/c and balb/c-h-2b mice |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2190061/ https://www.ncbi.nlm.nih.gov/pubmed/1194854 |