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Role of IL-13 in regulation of anti-tumor immunity and tumor growth

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Abstract

Major mediators of anti-tumor immunity are CD4+ T h 1 cells and CD8+ cytotoxic T lymphocytes (CTLs). In tumor-bearing animals, the T h 1- and CTL-mediated anti-tumor immunity is down-regulated in multiple ways. Better understanding of negative regulatory pathways of tumor immunity is crucial for the development of anti-tumor vaccines and immunotherapies. Since immune deviation toward T h 2 suppresses T h 1 development, it has been thought that induction affecting a T h 2 immune response is one of the mechanisms that down-regulate effective tumor immune responses. Recent studies using T h 2-deficient signal transducer and activator (Stat6) KO mice demonstrated that this hypothesis was the case. IL-13 is one of the T h 2 cytokines that has very similar features to IL-4 through sharing some receptor components and Stat6 signal transduction. It has been thought that IL-13 is not as critical for immune deviation as IL-4 since it cannot directly act on T cells. However, recent studies of IL-13 reveal that this cytokine plays a critical role in many aspects of immune regulation. Studies from our lab and others indicate that IL-13 is central to a novel immunoregulatory pathway in which NKT cells suppress tumor immunosurveillance. Here we will describe biological properties and functions of IL-13, its role in the negative regulation of anti-tumor immunity, and effects of IL-13 on tumor cells themselves.

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Correspondence to Masaki Terabe.

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This article forms part of the Symposium in Writing “Inhibitors of immunosurveillance and anti-tumor immunity,” published in Vol. 53.

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Terabe, M., Park, J.M. & Berzofsky, J.A. Role of IL-13 in regulation of anti-tumor immunity and tumor growth. Cancer Immunol Immunother 53, 79–85 (2004). https://doi.org/10.1007/s00262-003-0445-0

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