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CD11b(+)Ly6C(++)Ly6G(-) cells show distinct function in mice with chronic inflammation or tumor burden
BACKGROUND: S100A9 has been shown to be important for the function of so called Myeloid Derived Suppressor Cells (MDSC). Cells with a similar phenotype are also involved in pro-inflammatory processes, and we therefore wanted to investigate the gene expression and function of these cells in animals t...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3541244/ https://www.ncbi.nlm.nih.gov/pubmed/23234398 http://dx.doi.org/10.1186/1471-2172-13-69 |
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author | Källberg, Eva Stenström, Martin Liberg, David Ivars, Fredrik Leanderson, Tomas |
author_facet | Källberg, Eva Stenström, Martin Liberg, David Ivars, Fredrik Leanderson, Tomas |
author_sort | Källberg, Eva |
collection | PubMed |
description | BACKGROUND: S100A9 has been shown to be important for the function of so called Myeloid Derived Suppressor Cells (MDSC). Cells with a similar phenotype are also involved in pro-inflammatory processes, and we therefore wanted to investigate the gene expression and function of these cells in animals that were either subjected to chronic inflammation, or inoculated with tumors. METHODS: CD11b(+)Ly6C(++) and Ly6G(+) cells were isolated from spleen, tumor tissue or inflammatory granulomas. S100A9, Arginase 1 and iNOS gene expression in the various CD11b(+) cell populations was analyzed using Q-PCR. The suppressive activity of the CD11b(+) cell populations from different donors was studied in co-culture experiments. RESULTS: S100A9 was shown to be expressed mainly in splenic CD11b(+)Ly6C(+)G(+) cells both at the RNA and protein level. Arginase I and iNOS expression could be detected in both CD11b(+)Ly6C(+)Ly6G(+) and CD11b(+)Ly6C(+)G(-)/C(++)G(-) derived from tumors or a site of chronic inflammation, but was very low in the same cell populations isolated from the spleen. CD11b(+) cells isolated from mice with peritoneal chronic inflammation were able to stimulate T lymphocytes, while CD11b(+) cells from mice with peritoneal tumors suppressed T cell growth. CONCLUSION: An identical CD11b(+)Ly6C(++)G(-) cell population appears to have the ability to adopt immune stimulatory or immune suppressive functions dependent on the presence of a local inflammatory or tumor microenvironment. Thus, there is a functional plasticity in the CD11b(+)Ly6C(++)G(-) cell population that cannot be distinguished with the current molecular markers. |
format | Online Article Text |
id | pubmed-3541244 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-35412442013-01-11 CD11b(+)Ly6C(++)Ly6G(-) cells show distinct function in mice with chronic inflammation or tumor burden Källberg, Eva Stenström, Martin Liberg, David Ivars, Fredrik Leanderson, Tomas BMC Immunol Research Article BACKGROUND: S100A9 has been shown to be important for the function of so called Myeloid Derived Suppressor Cells (MDSC). Cells with a similar phenotype are also involved in pro-inflammatory processes, and we therefore wanted to investigate the gene expression and function of these cells in animals that were either subjected to chronic inflammation, or inoculated with tumors. METHODS: CD11b(+)Ly6C(++) and Ly6G(+) cells were isolated from spleen, tumor tissue or inflammatory granulomas. S100A9, Arginase 1 and iNOS gene expression in the various CD11b(+) cell populations was analyzed using Q-PCR. The suppressive activity of the CD11b(+) cell populations from different donors was studied in co-culture experiments. RESULTS: S100A9 was shown to be expressed mainly in splenic CD11b(+)Ly6C(+)G(+) cells both at the RNA and protein level. Arginase I and iNOS expression could be detected in both CD11b(+)Ly6C(+)Ly6G(+) and CD11b(+)Ly6C(+)G(-)/C(++)G(-) derived from tumors or a site of chronic inflammation, but was very low in the same cell populations isolated from the spleen. CD11b(+) cells isolated from mice with peritoneal chronic inflammation were able to stimulate T lymphocytes, while CD11b(+) cells from mice with peritoneal tumors suppressed T cell growth. CONCLUSION: An identical CD11b(+)Ly6C(++)G(-) cell population appears to have the ability to adopt immune stimulatory or immune suppressive functions dependent on the presence of a local inflammatory or tumor microenvironment. Thus, there is a functional plasticity in the CD11b(+)Ly6C(++)G(-) cell population that cannot be distinguished with the current molecular markers. BioMed Central 2012-12-12 /pmc/articles/PMC3541244/ /pubmed/23234398 http://dx.doi.org/10.1186/1471-2172-13-69 Text en Copyright ©2012 Kallberg et al.; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Källberg, Eva Stenström, Martin Liberg, David Ivars, Fredrik Leanderson, Tomas CD11b(+)Ly6C(++)Ly6G(-) cells show distinct function in mice with chronic inflammation or tumor burden |
title | CD11b(+)Ly6C(++)Ly6G(-) cells show distinct function in mice with chronic inflammation or tumor burden |
title_full | CD11b(+)Ly6C(++)Ly6G(-) cells show distinct function in mice with chronic inflammation or tumor burden |
title_fullStr | CD11b(+)Ly6C(++)Ly6G(-) cells show distinct function in mice with chronic inflammation or tumor burden |
title_full_unstemmed | CD11b(+)Ly6C(++)Ly6G(-) cells show distinct function in mice with chronic inflammation or tumor burden |
title_short | CD11b(+)Ly6C(++)Ly6G(-) cells show distinct function in mice with chronic inflammation or tumor burden |
title_sort | cd11b(+)ly6c(++)ly6g(-) cells show distinct function in mice with chronic inflammation or tumor burden |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3541244/ https://www.ncbi.nlm.nih.gov/pubmed/23234398 http://dx.doi.org/10.1186/1471-2172-13-69 |
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