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Open Access Highly Accessed Research article

CD11b+Ly6C++Ly6G- cells show distinct function in mice with chronic inflammation or tumor burden

Eva Källberg, Martin Stenström, David Liberg, Fredrik Ivars and Tomas Leanderson*

Author Affiliations

Immunology Group, Lund University and Active Biotech AB*, BMC D14, SE-22184, Lund, Sweden

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BMC Immunology 2012, 13:69  doi:10.1186/1471-2172-13-69

Published: 12 December 2012

Abstract

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.

Keywords:
Tumor; Inflammation; Myeloid cells; T cells; Suppression