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Peritoneal Cavity Is Dominated by IFNγ-Secreting CXCR3(+) Th1 Cells

The chemokine receptor CXCR3, which was shown to take part in many inflammatory processes, is considered as a Th1 specific marker. Here, we show in a mouse model that CXCR3 expressing CD4(+) cells preferentially migrate to the peritoneal cavity under steady-state conditions. The peritoneal cavity mi...

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Detalles Bibliográficos
Autores principales: Zygmunt, Beata M., Groebe, Lothar, Guzman, Carlos A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3138734/
https://www.ncbi.nlm.nih.gov/pubmed/21789162
http://dx.doi.org/10.1371/journal.pone.0018032
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author Zygmunt, Beata M.
Groebe, Lothar
Guzman, Carlos A.
author_facet Zygmunt, Beata M.
Groebe, Lothar
Guzman, Carlos A.
author_sort Zygmunt, Beata M.
collection PubMed
description The chemokine receptor CXCR3, which was shown to take part in many inflammatory processes, is considered as a Th1 specific marker. Here, we show in a mouse model that CXCR3 expressing CD4(+) cells preferentially migrate to the peritoneal cavity under steady-state conditions. The peritoneal cavity milieu leads to an up-regulated expression of CXCR3. However, blocking of known ligands of this chemokine receptor did not alter the preferential migration. The peritoneal cavity environment also results in an increased percentage of memory cells producing cytokines. Up-regulation of IFNγ production occurs mostly in CXCR3(+) cells considered as Th1, whereas the up-regulation of IL-4 affects mostly in CXCR3(−) cells which are considered as Th2. We conclude that the peritoneal cavity does not change the Th-lineage of the cells, but that domination of this anatomic niche by Th1 cells rather results from preferential migration to this compartment.
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spelling pubmed-31387342011-07-25 Peritoneal Cavity Is Dominated by IFNγ-Secreting CXCR3(+) Th1 Cells Zygmunt, Beata M. Groebe, Lothar Guzman, Carlos A. PLoS One Research Article The chemokine receptor CXCR3, which was shown to take part in many inflammatory processes, is considered as a Th1 specific marker. Here, we show in a mouse model that CXCR3 expressing CD4(+) cells preferentially migrate to the peritoneal cavity under steady-state conditions. The peritoneal cavity milieu leads to an up-regulated expression of CXCR3. However, blocking of known ligands of this chemokine receptor did not alter the preferential migration. The peritoneal cavity environment also results in an increased percentage of memory cells producing cytokines. Up-regulation of IFNγ production occurs mostly in CXCR3(+) cells considered as Th1, whereas the up-regulation of IL-4 affects mostly in CXCR3(−) cells which are considered as Th2. We conclude that the peritoneal cavity does not change the Th-lineage of the cells, but that domination of this anatomic niche by Th1 cells rather results from preferential migration to this compartment. Public Library of Science 2011-07-18 /pmc/articles/PMC3138734/ /pubmed/21789162 http://dx.doi.org/10.1371/journal.pone.0018032 Text en Zygmunt et al. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
Zygmunt, Beata M.
Groebe, Lothar
Guzman, Carlos A.
Peritoneal Cavity Is Dominated by IFNγ-Secreting CXCR3(+) Th1 Cells
title Peritoneal Cavity Is Dominated by IFNγ-Secreting CXCR3(+) Th1 Cells
title_full Peritoneal Cavity Is Dominated by IFNγ-Secreting CXCR3(+) Th1 Cells
title_fullStr Peritoneal Cavity Is Dominated by IFNγ-Secreting CXCR3(+) Th1 Cells
title_full_unstemmed Peritoneal Cavity Is Dominated by IFNγ-Secreting CXCR3(+) Th1 Cells
title_short Peritoneal Cavity Is Dominated by IFNγ-Secreting CXCR3(+) Th1 Cells
title_sort peritoneal cavity is dominated by ifnγ-secreting cxcr3(+) th1 cells
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3138734/
https://www.ncbi.nlm.nih.gov/pubmed/21789162
http://dx.doi.org/10.1371/journal.pone.0018032
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