Journal
NATURE COMMUNICATIONS
Volume 2, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ncomms1239
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Funding
- Anders Jahre fund
- Henrik Homans Minde fund
- Legat for fremme av kreftforskningen
- Familien Blix fond til fremme for medisinsk forskning
- S.G. Sonneland Foundation
- Andrine og Hans Gysler Berg fund
- Multiple Myeloma Research Foundation
- Helse Sor-Ost
- Research Council of Norway
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The immune system can both promote and suppress cancer. Chronic inflammation and proinflammatory cytokines such as interleukin (IL)-1 and IL-6 are considered to be tumour promoting. In contrast, the exact nature of protective antitumour immunity remains obscure. Here, we quantify locally secreted cytokines during primary immune responses against myeloma and B-cell lymphoma in mice. Strikingly, successful cancer immunosurveillance mediated by tumour-specific CD4(+) T cells is consistently associated with elevated local levels of both proinflammatory (IL-1 alpha, IL-1 beta and IL-6) and T helper 1 (Th1)-associated cytokines (interferon-gamma (IFN-gamma), IL-2 and IL-12). Cancer eradication is achieved by a collaboration between tumour-specific Th1 cells and tumour-infiltrating, antigen-presenting macrophages. Th1 cells induce secretion of IL-1 beta and IL-6 by macrophages. Th1-derived IFN-gamma is shown to render macrophages directly cytotoxic to cancer cells, and to induce macrophages to secrete the angiostatic chemokines CXCL9/MIG and CXCL10/IP-10. Thus, inflammation, when driven by tumour-specific Th1 cells, may prevent rather than promote cancer.
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