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CCR7 ligands control basal T cell motility within lymph node slices in a phosphoinositide 3–kinase– independent manner
The molecular mechanisms responsible for the sustained basal motility of T cells within lymph nodes (LNs) remain elusive. To study T cell motility in a LN environment, we have developed a new experimental system based on slices of LNs that allows the assessment of T cell trafficking after adoptive t...
Autores principales: | , , , , |
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Formato: | Texto |
Lenguaje: | English |
Publicado: |
The Rockefeller University Press
2007
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2118589/ https://www.ncbi.nlm.nih.gov/pubmed/17485513 http://dx.doi.org/10.1084/jem.20062079 |
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author | Asperti-Boursin, François Real, Eliana Bismuth, Georges Trautmann, Alain Donnadieu, Emmanuel |
author_facet | Asperti-Boursin, François Real, Eliana Bismuth, Georges Trautmann, Alain Donnadieu, Emmanuel |
author_sort | Asperti-Boursin, François |
collection | PubMed |
description | The molecular mechanisms responsible for the sustained basal motility of T cells within lymph nodes (LNs) remain elusive. To study T cell motility in a LN environment, we have developed a new experimental system based on slices of LNs that allows the assessment of T cell trafficking after adoptive transfer or direct addition of T cells to the slice. Using this experimental system, we show that T cell motility is highly sensitive to pertussis toxin and strongly depends on CCR7 and its ligands. Our results also demonstrate that, despite its established role in myeloid cell locomotion, phosphoinositide 3–kinase (PI3K) activity does not contribute to the exploratory behavior of the T lymphocytes within LN slices. Likewise, although PI3K activation is detectable in chemokine-treated T cells, PI3K plays only a minor role in T cell polarization and migration in vitro. Collectively, our results suggest that the common amplification system that, in other cells, facilitates large phosphatidylinositol 3,4,5-trisphosphate increases at the plasma membrane is absent in T cells. We conclude that T cell motility within LNs is not an intrinsic property of T lymphocytes but is driven in a PI3K-independent manner by the lymphoid chemokine-rich environment. |
format | Text |
id | pubmed-2118589 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2007 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-21185892007-12-13 CCR7 ligands control basal T cell motility within lymph node slices in a phosphoinositide 3–kinase– independent manner Asperti-Boursin, François Real, Eliana Bismuth, Georges Trautmann, Alain Donnadieu, Emmanuel J Exp Med Articles The molecular mechanisms responsible for the sustained basal motility of T cells within lymph nodes (LNs) remain elusive. To study T cell motility in a LN environment, we have developed a new experimental system based on slices of LNs that allows the assessment of T cell trafficking after adoptive transfer or direct addition of T cells to the slice. Using this experimental system, we show that T cell motility is highly sensitive to pertussis toxin and strongly depends on CCR7 and its ligands. Our results also demonstrate that, despite its established role in myeloid cell locomotion, phosphoinositide 3–kinase (PI3K) activity does not contribute to the exploratory behavior of the T lymphocytes within LN slices. Likewise, although PI3K activation is detectable in chemokine-treated T cells, PI3K plays only a minor role in T cell polarization and migration in vitro. Collectively, our results suggest that the common amplification system that, in other cells, facilitates large phosphatidylinositol 3,4,5-trisphosphate increases at the plasma membrane is absent in T cells. We conclude that T cell motility within LNs is not an intrinsic property of T lymphocytes but is driven in a PI3K-independent manner by the lymphoid chemokine-rich environment. The Rockefeller University Press 2007-05-14 /pmc/articles/PMC2118589/ /pubmed/17485513 http://dx.doi.org/10.1084/jem.20062079 Text en Copyright © 2007, The Rockefeller University Press 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 Asperti-Boursin, François Real, Eliana Bismuth, Georges Trautmann, Alain Donnadieu, Emmanuel CCR7 ligands control basal T cell motility within lymph node slices in a phosphoinositide 3–kinase– independent manner |
title | CCR7 ligands control basal T cell motility within lymph node slices in a phosphoinositide 3–kinase– independent manner |
title_full | CCR7 ligands control basal T cell motility within lymph node slices in a phosphoinositide 3–kinase– independent manner |
title_fullStr | CCR7 ligands control basal T cell motility within lymph node slices in a phosphoinositide 3–kinase– independent manner |
title_full_unstemmed | CCR7 ligands control basal T cell motility within lymph node slices in a phosphoinositide 3–kinase– independent manner |
title_short | CCR7 ligands control basal T cell motility within lymph node slices in a phosphoinositide 3–kinase– independent manner |
title_sort | ccr7 ligands control basal t cell motility within lymph node slices in a phosphoinositide 3–kinase– independent manner |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2118589/ https://www.ncbi.nlm.nih.gov/pubmed/17485513 http://dx.doi.org/10.1084/jem.20062079 |
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