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The polarization of immune cells in the tumour environment by TGFβ

The polarization of immune cells in the tumour environment by TGFβ During early tumour formation, transforming growth factor-β (TGFβ) can function as a tumour suppressor to prevent tumorigenesis; however, overproduction of TGFβ in established tumours is often associated with tumour metastasis and poor prognosis in patients with cancer. The tumour-promoting effects of TGFβ may be due to the immunosuppressive effects it has on both innate and adaptive immunity. TGFβ inhibits natural killer cell function by inhibiting cytokine production and downregulating the expression of activating receptors. TGFβ inhibits the maturation of, and cytokine production and proper antigen presentation by, dendritic cells, while promoting regulatory T (TReg) cell differentiation and an overall tolerogenic state. TGFβ also promotes an M2 phenotype for macrophages and an N2 phenotype for neutrophils. TGFβ directly dampens the function of CD4+ and CD8+ effector T cells and promotes the survival of TReg cells. Depending on the cytokine milieu, TGFβ greatly affects the differentiation of several key CD4+ T cell subsets in tumour immunology. There is great interest in targeting TGFβ-induced signalling for immunotherapy of cancer; however, the dosing, timing and combination of this approach with other immunotherapies to achieve the most successful antitumour effect need to be further investigated. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Nature Reviews Immunology Springer Journals

The polarization of immune cells in the tumour environment by TGFβ

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References (169)

Publisher
Springer Journals
Copyright
Copyright © 2010 by Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.
Subject
Biomedicine; Biomedicine, general; Immunology
ISSN
1474-1733
eISSN
1474-1741
DOI
10.1038/nri2808
Publisher site
See Article on Publisher Site

Abstract

During early tumour formation, transforming growth factor-β (TGFβ) can function as a tumour suppressor to prevent tumorigenesis; however, overproduction of TGFβ in established tumours is often associated with tumour metastasis and poor prognosis in patients with cancer. The tumour-promoting effects of TGFβ may be due to the immunosuppressive effects it has on both innate and adaptive immunity. TGFβ inhibits natural killer cell function by inhibiting cytokine production and downregulating the expression of activating receptors. TGFβ inhibits the maturation of, and cytokine production and proper antigen presentation by, dendritic cells, while promoting regulatory T (TReg) cell differentiation and an overall tolerogenic state. TGFβ also promotes an M2 phenotype for macrophages and an N2 phenotype for neutrophils. TGFβ directly dampens the function of CD4+ and CD8+ effector T cells and promotes the survival of TReg cells. Depending on the cytokine milieu, TGFβ greatly affects the differentiation of several key CD4+ T cell subsets in tumour immunology. There is great interest in targeting TGFβ-induced signalling for immunotherapy of cancer; however, the dosing, timing and combination of this approach with other immunotherapies to achieve the most successful antitumour effect need to be further investigated.

Journal

Nature Reviews Immunology – Springer Journals

Published: Jul 9, 2010

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