Th2-mediated anti-tumour immunity: friend or foe?

Authors

  • J. I. Ellyard,

    1. Cancer and Vascular Biology Group, Division of Immunology and Genetics, John Curtin School of Medical Research, Australian National University, Canberra, Australia
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  • L. Simson,

    1. Cancer and Vascular Biology Group, Division of Immunology and Genetics, John Curtin School of Medical Research, Australian National University, Canberra, Australia
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  • C. R. Parish

    Corresponding author
    1. Cancer and Vascular Biology Group, Division of Immunology and Genetics, John Curtin School of Medical Research, Australian National University, Canberra, Australia
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Christopher Parish, BAgrSci, PhD (Melb)
Cancer and Vascular Biology Group
Division of Immunology and Genetics
John Curtin School of Medical Research
Australian National University
PO Box 334
Canberra City, ACT 2601
Australia
Tel: +61 2 6125 2604
Fax: +61 2 6125 2595
e-mail: christopher.parish@anu.edu.au

Abstract

The concept that the immune system can recognise tumour cells and either eliminate them (tumour immune surveillance) or select for immunologically resistant variants (immunoediting) is gaining general acceptance by immunologists. In terms of an adaptive immune response to cancer, however, much of the research has focused on the response of cytotoxic CD8+ T lymphocytes to tumour-specific antigens and the production of Th1 cytokines by CD4+ and CD8+ T cells. In contrast, Th2-mediated immunity has traditionally been viewed as favouring tumour growth, both by promoting angiogenesis and by inhibiting cell-mediated immunity and subsequent tumour cell killing. While there is evidence that components of type 2 inflammation, such as B cells and interleukin-10, do promote tumour growth, there are also many studies demonstrating the anti-tumour activity of CD4+ Th2 cells, particularly in collaboration with tumour-infiltrating granulocytes, such as eosinophils. In this review, we examine all the components of type 2 immunity and their effects on tumour growth. Collectively, from this analysis, we conclude that there is a great potential for the development of Th2-mediated immunotherapies that harness the cytotoxic activity of eosinophils.

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