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T cell receptor V gene usage of islet beta cell-reactive T cells is not restricted in non-obese diabetic mice
Five islet-reactive T cell clones were established from islet- infiltrating T cells of non-obese diabetic (NOD) mice. All clones expressed CD4, but not CD8, and responded to islet cells from various strains of mice in the context of I-ANOD. They could induce insulitis when transferred into disease-r...
Formato: | Texto |
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Lenguaje: | English |
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The Rockefeller University Press
1991
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2118862/ https://www.ncbi.nlm.nih.gov/pubmed/1902501 |
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collection | PubMed |
description | Five islet-reactive T cell clones were established from islet- infiltrating T cells of non-obese diabetic (NOD) mice. All clones expressed CD4, but not CD8, and responded to islet cells from various strains of mice in the context of I-ANOD. They could induce insulitis when transferred into disease-resistant I-E+ transgenic NOD mice. The T cell receptor (TCR) sequences utilized by the clones were determined. Their usage of TCR V and J segments was not restricted but was rather diverse. One of the clones utilized V beta 16. The expression of V beta 16 was significantly reduced in I-E+ transgenic NOD, suggesting the possibility that the islet-reactive T cell clone expressing V beta 16 may be deleted or inactivated by I-E molecules. This clone might be one of the candidates that triggers insulitis. |
format | Text |
id | pubmed-2118862 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1991 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-21188622008-04-17 T cell receptor V gene usage of islet beta cell-reactive T cells is not restricted in non-obese diabetic mice J Exp Med Articles Five islet-reactive T cell clones were established from islet- infiltrating T cells of non-obese diabetic (NOD) mice. All clones expressed CD4, but not CD8, and responded to islet cells from various strains of mice in the context of I-ANOD. They could induce insulitis when transferred into disease-resistant I-E+ transgenic NOD mice. The T cell receptor (TCR) sequences utilized by the clones were determined. Their usage of TCR V and J segments was not restricted but was rather diverse. One of the clones utilized V beta 16. The expression of V beta 16 was significantly reduced in I-E+ transgenic NOD, suggesting the possibility that the islet-reactive T cell clone expressing V beta 16 may be deleted or inactivated by I-E molecules. This clone might be one of the candidates that triggers insulitis. The Rockefeller University Press 1991-05-01 /pmc/articles/PMC2118862/ /pubmed/1902501 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 T cell receptor V gene usage of islet beta cell-reactive T cells is not restricted in non-obese diabetic mice |
title | T cell receptor V gene usage of islet beta cell-reactive T cells is not restricted in non-obese diabetic mice |
title_full | T cell receptor V gene usage of islet beta cell-reactive T cells is not restricted in non-obese diabetic mice |
title_fullStr | T cell receptor V gene usage of islet beta cell-reactive T cells is not restricted in non-obese diabetic mice |
title_full_unstemmed | T cell receptor V gene usage of islet beta cell-reactive T cells is not restricted in non-obese diabetic mice |
title_short | T cell receptor V gene usage of islet beta cell-reactive T cells is not restricted in non-obese diabetic mice |
title_sort | t cell receptor v gene usage of islet beta cell-reactive t cells is not restricted in non-obese diabetic mice |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2118862/ https://www.ncbi.nlm.nih.gov/pubmed/1902501 |