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Oleate but not stearate induces the regulatory phenotype of myeloid suppressor cells

Tumor infiltrating myeloid cells play contradictory roles in the tumor development. Dendritic cells and classical activated macrophages support anti-tumor immune activity via antigen presentation and induction of pro-inflammatory immune responses. Myeloid suppressor cells (MSCs), for instance myeloi...

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Autores principales: Wu, Hao, Weidinger, Carl, Schmidt, Franziska, Keye, Jacqueline, Friedrich, Marie, Yerinde, Cansu, Willimsky, Gerald, Qin, Zhihai, Siegmund, Britta, Glauben, Rainer
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5548895/
https://www.ncbi.nlm.nih.gov/pubmed/28790345
http://dx.doi.org/10.1038/s41598-017-07685-9
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author Wu, Hao
Weidinger, Carl
Schmidt, Franziska
Keye, Jacqueline
Friedrich, Marie
Yerinde, Cansu
Willimsky, Gerald
Qin, Zhihai
Siegmund, Britta
Glauben, Rainer
author_facet Wu, Hao
Weidinger, Carl
Schmidt, Franziska
Keye, Jacqueline
Friedrich, Marie
Yerinde, Cansu
Willimsky, Gerald
Qin, Zhihai
Siegmund, Britta
Glauben, Rainer
author_sort Wu, Hao
collection PubMed
description Tumor infiltrating myeloid cells play contradictory roles in the tumor development. Dendritic cells and classical activated macrophages support anti-tumor immune activity via antigen presentation and induction of pro-inflammatory immune responses. Myeloid suppressor cells (MSCs), for instance myeloid derived suppressor cells (MDSCs) or tumor associated macrophages play a critical role in tumor growth. Here, treatment with sodium oleate, an unsaturated fatty acid, induced a regulatory phenotype in the myeloid suppressor cell line MSC-2 and resulted in an increased suppression of activated T cells, paralleled by increased intracellular lipid droplets formation. Furthermore, sodium oleate potentiated nitric oxide (NO) production in MSC-2, thereby increasing their suppressive capacity. In primary polarized bone marrow cells, sodium oleate (C18:1) and linoleate (C18:2), but not stearate (C18:0) were identified as potent FFA to induce a regulatory phenotype. This effect was abrogated in MSC-2 as well as primary cells by specific inhibition of droplets formation while the inhibition of de novo FFA synthesis proved ineffective, suggesting a critical role for exogenous FFA in the functional induction of MSCs. Taken together our data introduce a new unsaturated fatty acid-dependent pathway shaping the functional phenotype of MSCs, facilitating the tumor escape from the immune system.
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spelling pubmed-55488952017-08-09 Oleate but not stearate induces the regulatory phenotype of myeloid suppressor cells Wu, Hao Weidinger, Carl Schmidt, Franziska Keye, Jacqueline Friedrich, Marie Yerinde, Cansu Willimsky, Gerald Qin, Zhihai Siegmund, Britta Glauben, Rainer Sci Rep Article Tumor infiltrating myeloid cells play contradictory roles in the tumor development. Dendritic cells and classical activated macrophages support anti-tumor immune activity via antigen presentation and induction of pro-inflammatory immune responses. Myeloid suppressor cells (MSCs), for instance myeloid derived suppressor cells (MDSCs) or tumor associated macrophages play a critical role in tumor growth. Here, treatment with sodium oleate, an unsaturated fatty acid, induced a regulatory phenotype in the myeloid suppressor cell line MSC-2 and resulted in an increased suppression of activated T cells, paralleled by increased intracellular lipid droplets formation. Furthermore, sodium oleate potentiated nitric oxide (NO) production in MSC-2, thereby increasing their suppressive capacity. In primary polarized bone marrow cells, sodium oleate (C18:1) and linoleate (C18:2), but not stearate (C18:0) were identified as potent FFA to induce a regulatory phenotype. This effect was abrogated in MSC-2 as well as primary cells by specific inhibition of droplets formation while the inhibition of de novo FFA synthesis proved ineffective, suggesting a critical role for exogenous FFA in the functional induction of MSCs. Taken together our data introduce a new unsaturated fatty acid-dependent pathway shaping the functional phenotype of MSCs, facilitating the tumor escape from the immune system. Nature Publishing Group UK 2017-08-08 /pmc/articles/PMC5548895/ /pubmed/28790345 http://dx.doi.org/10.1038/s41598-017-07685-9 Text en © The Author(s) 2017 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Wu, Hao
Weidinger, Carl
Schmidt, Franziska
Keye, Jacqueline
Friedrich, Marie
Yerinde, Cansu
Willimsky, Gerald
Qin, Zhihai
Siegmund, Britta
Glauben, Rainer
Oleate but not stearate induces the regulatory phenotype of myeloid suppressor cells
title Oleate but not stearate induces the regulatory phenotype of myeloid suppressor cells
title_full Oleate but not stearate induces the regulatory phenotype of myeloid suppressor cells
title_fullStr Oleate but not stearate induces the regulatory phenotype of myeloid suppressor cells
title_full_unstemmed Oleate but not stearate induces the regulatory phenotype of myeloid suppressor cells
title_short Oleate but not stearate induces the regulatory phenotype of myeloid suppressor cells
title_sort oleate but not stearate induces the regulatory phenotype of myeloid suppressor cells
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5548895/
https://www.ncbi.nlm.nih.gov/pubmed/28790345
http://dx.doi.org/10.1038/s41598-017-07685-9
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