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Tumour cell conditioned medium reveals greater M2 skewing of macrophages in the absence of properdin
INTRODUCTION: The tumour microenvironment is shaped by the interaction of immune, non immune, and tumour cells present in close proximity. Tumour cells direct the development of a locally immune suppressed state, affecting the activity of anti tumour T cells and preparing the escape phase of tumour...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5322164/ https://www.ncbi.nlm.nih.gov/pubmed/28250926 http://dx.doi.org/10.1002/iid3.142 |
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author | Al‐Rayahi, Izzat A.M. Browning, Michael J. Stover, Cordula |
author_facet | Al‐Rayahi, Izzat A.M. Browning, Michael J. Stover, Cordula |
author_sort | Al‐Rayahi, Izzat A.M. |
collection | PubMed |
description | INTRODUCTION: The tumour microenvironment is shaped by the interaction of immune, non immune, and tumour cells present in close proximity. Tumour cells direct the development of a locally immune suppressed state, affecting the activity of anti tumour T cells and preparing the escape phase of tumour development. Macrophages in the tumour typically develop into so‐called tumour associated macrophages with a distinct profile of activities which lead to a reduction in inflammation and antigen presentation. The direct impact of tumour cell conditioned medium on the activity profile of macrophages in dependence of their complement component expression has not yet been investigated. METHODS: In our in vitro study, macrophages differentiated from bone marrows of properdin deficient and wildtype mice were stimulated with conditioned medium of a syngeneic tumour cell line, B16F10, a mouse melanoma subline. RESULTS: In comparison with macrophages from wildtype mice, those from congenic properdin deficient mice showed skewing towards M2 profile, encompassing mRNA expression for genes involved in arginine metabolism, production of type 2 cytokines, and relatively lower surface expression of molecules needed for antigen presentation. CONCLUSIONS: These data suggest that properdin insufficiency promotes a tumour environment that helps the tumour evade the immune response. |
format | Online Article Text |
id | pubmed-5322164 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-53221642017-03-01 Tumour cell conditioned medium reveals greater M2 skewing of macrophages in the absence of properdin Al‐Rayahi, Izzat A.M. Browning, Michael J. Stover, Cordula Immun Inflamm Dis Original Research INTRODUCTION: The tumour microenvironment is shaped by the interaction of immune, non immune, and tumour cells present in close proximity. Tumour cells direct the development of a locally immune suppressed state, affecting the activity of anti tumour T cells and preparing the escape phase of tumour development. Macrophages in the tumour typically develop into so‐called tumour associated macrophages with a distinct profile of activities which lead to a reduction in inflammation and antigen presentation. The direct impact of tumour cell conditioned medium on the activity profile of macrophages in dependence of their complement component expression has not yet been investigated. METHODS: In our in vitro study, macrophages differentiated from bone marrows of properdin deficient and wildtype mice were stimulated with conditioned medium of a syngeneic tumour cell line, B16F10, a mouse melanoma subline. RESULTS: In comparison with macrophages from wildtype mice, those from congenic properdin deficient mice showed skewing towards M2 profile, encompassing mRNA expression for genes involved in arginine metabolism, production of type 2 cytokines, and relatively lower surface expression of molecules needed for antigen presentation. CONCLUSIONS: These data suggest that properdin insufficiency promotes a tumour environment that helps the tumour evade the immune response. John Wiley and Sons Inc. 2017-01-26 /pmc/articles/PMC5322164/ /pubmed/28250926 http://dx.doi.org/10.1002/iid3.142 Text en © 2017 The Authors. Immunity, Inflammation and Disease Published by John Wiley & Sons Ltd. This is an open access article under the terms of the Creative Commons Attribution (http://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Research Al‐Rayahi, Izzat A.M. Browning, Michael J. Stover, Cordula Tumour cell conditioned medium reveals greater M2 skewing of macrophages in the absence of properdin |
title | Tumour cell conditioned medium reveals greater M2 skewing of macrophages in the absence of properdin |
title_full | Tumour cell conditioned medium reveals greater M2 skewing of macrophages in the absence of properdin |
title_fullStr | Tumour cell conditioned medium reveals greater M2 skewing of macrophages in the absence of properdin |
title_full_unstemmed | Tumour cell conditioned medium reveals greater M2 skewing of macrophages in the absence of properdin |
title_short | Tumour cell conditioned medium reveals greater M2 skewing of macrophages in the absence of properdin |
title_sort | tumour cell conditioned medium reveals greater m2 skewing of macrophages in the absence of properdin |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5322164/ https://www.ncbi.nlm.nih.gov/pubmed/28250926 http://dx.doi.org/10.1002/iid3.142 |
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