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Bacterial superantigens mediate T cell deletions in the mouse severe combined immunodeficiency-human liver/thymus model
The ability to analyze T cell receptor (TCR) thymic repertoire shaping in humans by self and foreign ligands is hampered by the lack of suitable models. We recently documented that the mouse severe combined immunodeficiency (SCID)-human fetal liver/thymus model recapitulates the TCR V beta gene repe...
Formato: | Texto |
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Lenguaje: | English |
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The Rockefeller University Press
1993
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2190996/ https://www.ncbi.nlm.nih.gov/pubmed/8478618 |
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collection | PubMed |
description | The ability to analyze T cell receptor (TCR) thymic repertoire shaping in humans by self and foreign ligands is hampered by the lack of suitable models. We recently documented that the mouse severe combined immunodeficiency (SCID)-human fetal liver/thymus model recapitulates the TCR V beta gene repertoire of human thymocytes. Here, we show that an exogenous superantigen, staphylococcal enterotoxin B, administered to such mice induces clonal deletions in both CD4+8- and CD8+4- cells involving the same human V beta clones that are selected in vitro by this toxin. This model, therefore, may allow comprehensive studies into the effects of microbial and other agents on human T cell thymic selection processes in a biologically relevant setting. |
format | Text |
id | pubmed-2190996 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1993 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-21909962008-04-16 Bacterial superantigens mediate T cell deletions in the mouse severe combined immunodeficiency-human liver/thymus model J Exp Med Articles The ability to analyze T cell receptor (TCR) thymic repertoire shaping in humans by self and foreign ligands is hampered by the lack of suitable models. We recently documented that the mouse severe combined immunodeficiency (SCID)-human fetal liver/thymus model recapitulates the TCR V beta gene repertoire of human thymocytes. Here, we show that an exogenous superantigen, staphylococcal enterotoxin B, administered to such mice induces clonal deletions in both CD4+8- and CD8+4- cells involving the same human V beta clones that are selected in vitro by this toxin. This model, therefore, may allow comprehensive studies into the effects of microbial and other agents on human T cell thymic selection processes in a biologically relevant setting. The Rockefeller University Press 1993-05-01 /pmc/articles/PMC2190996/ /pubmed/8478618 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 Bacterial superantigens mediate T cell deletions in the mouse severe combined immunodeficiency-human liver/thymus model |
title | Bacterial superantigens mediate T cell deletions in the mouse severe combined immunodeficiency-human liver/thymus model |
title_full | Bacterial superantigens mediate T cell deletions in the mouse severe combined immunodeficiency-human liver/thymus model |
title_fullStr | Bacterial superantigens mediate T cell deletions in the mouse severe combined immunodeficiency-human liver/thymus model |
title_full_unstemmed | Bacterial superantigens mediate T cell deletions in the mouse severe combined immunodeficiency-human liver/thymus model |
title_short | Bacterial superantigens mediate T cell deletions in the mouse severe combined immunodeficiency-human liver/thymus model |
title_sort | bacterial superantigens mediate t cell deletions in the mouse severe combined immunodeficiency-human liver/thymus model |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2190996/ https://www.ncbi.nlm.nih.gov/pubmed/8478618 |