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Genetically determined lack of CD45R- T cells in healthy individuals. Evidence for a regulatory polymorphism of CD45R antigen expression
A genetic polymorphism of CD45R expression was identified resulting in a lack of CD45R- lymphocytes in approximately 8% of healthy individuals. Family studies revealed an autosomal dominant mode of inheritance of the variant CD45R expression pattern. PBMC from donors possessing the variant type did...
Formato: | Texto |
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Lenguaje: | English |
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The Rockefeller University Press
1990
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2187890/ https://www.ncbi.nlm.nih.gov/pubmed/1692083 |
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collection | PubMed |
description | A genetic polymorphism of CD45R expression was identified resulting in a lack of CD45R- lymphocytes in approximately 8% of healthy individuals. Family studies revealed an autosomal dominant mode of inheritance of the variant CD45R expression pattern. PBMC from donors possessing the variant type did not lose the CD45R antigen after in vitro activation, whereas a decrease of CD45R molecules was readily detected in individuals with the normal pattern. The expression of CD45RO antigens, as well as memory cell function, did not differ between both groups. These data show that activation and in vivo priming of T cells is not necessarily associated with a loss of CD45R antigen expression. |
format | Text |
id | pubmed-2187890 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1990 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-21878902008-04-17 Genetically determined lack of CD45R- T cells in healthy individuals. Evidence for a regulatory polymorphism of CD45R antigen expression J Exp Med Articles A genetic polymorphism of CD45R expression was identified resulting in a lack of CD45R- lymphocytes in approximately 8% of healthy individuals. Family studies revealed an autosomal dominant mode of inheritance of the variant CD45R expression pattern. PBMC from donors possessing the variant type did not lose the CD45R antigen after in vitro activation, whereas a decrease of CD45R molecules was readily detected in individuals with the normal pattern. The expression of CD45RO antigens, as well as memory cell function, did not differ between both groups. These data show that activation and in vivo priming of T cells is not necessarily associated with a loss of CD45R antigen expression. The Rockefeller University Press 1990-05-01 /pmc/articles/PMC2187890/ /pubmed/1692083 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 Genetically determined lack of CD45R- T cells in healthy individuals. Evidence for a regulatory polymorphism of CD45R antigen expression |
title | Genetically determined lack of CD45R- T cells in healthy individuals. Evidence for a regulatory polymorphism of CD45R antigen expression |
title_full | Genetically determined lack of CD45R- T cells in healthy individuals. Evidence for a regulatory polymorphism of CD45R antigen expression |
title_fullStr | Genetically determined lack of CD45R- T cells in healthy individuals. Evidence for a regulatory polymorphism of CD45R antigen expression |
title_full_unstemmed | Genetically determined lack of CD45R- T cells in healthy individuals. Evidence for a regulatory polymorphism of CD45R antigen expression |
title_short | Genetically determined lack of CD45R- T cells in healthy individuals. Evidence for a regulatory polymorphism of CD45R antigen expression |
title_sort | genetically determined lack of cd45r- t cells in healthy individuals. evidence for a regulatory polymorphism of cd45r antigen expression |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2187890/ https://www.ncbi.nlm.nih.gov/pubmed/1692083 |