Please use this identifier to cite or link to this item: http://hdl.handle.net/2381/39407
Title: Tumour cell conditioned medium reveals greater M2 skewing of macrophages in the absence of properdin.
Authors: Al-Rayahi, Izzat A.M.
Browning, Michael J.
Stover, Cordula
First Published: 26-Jan-2017
Publisher: Wiley
Citation: Immunity, Inflammation and Disease, 2017, 5 (1), pp. 68-77
Abstract: 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.
DOI Link: 10.1002/iid3.142
eISSN: 2050-4527
Links: http://onlinelibrary.wiley.com/doi/10.1002/iid3.142/abstract
http://hdl.handle.net/2381/39407
Version: Publisher Version
Status: Peer-reviewed
Type: Journal Article
Rights: © 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 License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
Appears in Collections:Published Articles, Dept. of Infection, Immunity and Inflammation

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