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Cytotoxic T lymphocytes from HLA-A2 transgenic mice specific for HLA-A2 expressed on human cells
CTL clones were derived from HLA-A2.1 transgenic mice by immunization with a human cell expressing HLA-A2.1. None of these clones lysed murine transfectants, and only 3 of 23 lysed monkey transfectants expressing HLA-A2. In contrast, all of these clones lysed a wide variety of human cells expressing...
Formato: | Texto |
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Lenguaje: | English |
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The Rockefeller University Press
1988
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2189026/ https://www.ncbi.nlm.nih.gov/pubmed/3262704 |
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collection | PubMed |
description | CTL clones were derived from HLA-A2.1 transgenic mice by immunization with a human cell expressing HLA-A2.1. None of these clones lysed murine transfectants, and only 3 of 23 lysed monkey transfectants expressing HLA-A2. In contrast, all of these clones lysed a wide variety of human cells expressing HLA-A2.1. These results demonstrate the existence of species-specific epitopes on the HLA-A2.1 molecule, and suggest that these epitopes are formed by the association of class I MHC products with one or more endogenous species-specific molecules. These results provide an explanation for the frequently observed failure of HLA class I-specific CTL to recognize these antigens on murine transfectants. These results also suggest that such endogenous proteins may also contribute to the formation of epitopes recognized by allospecific CTL. |
format | Text |
id | pubmed-2189026 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1988 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-21890262008-04-17 Cytotoxic T lymphocytes from HLA-A2 transgenic mice specific for HLA-A2 expressed on human cells J Exp Med Articles CTL clones were derived from HLA-A2.1 transgenic mice by immunization with a human cell expressing HLA-A2.1. None of these clones lysed murine transfectants, and only 3 of 23 lysed monkey transfectants expressing HLA-A2. In contrast, all of these clones lysed a wide variety of human cells expressing HLA-A2.1. These results demonstrate the existence of species-specific epitopes on the HLA-A2.1 molecule, and suggest that these epitopes are formed by the association of class I MHC products with one or more endogenous species-specific molecules. These results provide an explanation for the frequently observed failure of HLA class I-specific CTL to recognize these antigens on murine transfectants. These results also suggest that such endogenous proteins may also contribute to the formation of epitopes recognized by allospecific CTL. The Rockefeller University Press 1988-09-01 /pmc/articles/PMC2189026/ /pubmed/3262704 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 Cytotoxic T lymphocytes from HLA-A2 transgenic mice specific for HLA-A2 expressed on human cells |
title | Cytotoxic T lymphocytes from HLA-A2 transgenic mice specific for HLA-A2 expressed on human cells |
title_full | Cytotoxic T lymphocytes from HLA-A2 transgenic mice specific for HLA-A2 expressed on human cells |
title_fullStr | Cytotoxic T lymphocytes from HLA-A2 transgenic mice specific for HLA-A2 expressed on human cells |
title_full_unstemmed | Cytotoxic T lymphocytes from HLA-A2 transgenic mice specific for HLA-A2 expressed on human cells |
title_short | Cytotoxic T lymphocytes from HLA-A2 transgenic mice specific for HLA-A2 expressed on human cells |
title_sort | cytotoxic t lymphocytes from hla-a2 transgenic mice specific for hla-a2 expressed on human cells |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2189026/ https://www.ncbi.nlm.nih.gov/pubmed/3262704 |