Inflammation driven by tumour-specific Th1 cells protects against B-cell cancer

Ole Audun Werner Haabeth, Kristina Berg Lorvik, Clara Hammarström, Ian M. Donaldson, Guttorm Haraldsen, Bjarne Bogen and Alexandre Corthay ()
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Ole Audun Werner Haabeth: Centre for Immune Regulation, Institute of Immunology, University of Oslo and Oslo University Hospital Rikshospitalet, PO Box 4950 Nydalen, 0424 Oslo, Norway.
Kristina Berg Lorvik: Centre for Immune Regulation, Institute of Immunology, University of Oslo and Oslo University Hospital Rikshospitalet, PO Box 4950 Nydalen, 0424 Oslo, Norway.
Clara Hammarström: Institute of Pathology, Oslo University Hospital Rikshospitalet and University of Oslo, PO Box 4950 Nydalen, 0424 Oslo, Norway.
Ian M. Donaldson: The Biotechnology Centre of Oslo, University of Oslo, PO Box 1125 Blindern, 0317 Oslo, Norway.
Guttorm Haraldsen: Institute of Pathology, Oslo University Hospital Rikshospitalet and University of Oslo, PO Box 4950 Nydalen, 0424 Oslo, Norway.
Bjarne Bogen: Centre for Immune Regulation, Institute of Immunology, University of Oslo and Oslo University Hospital Rikshospitalet, PO Box 4950 Nydalen, 0424 Oslo, Norway.
Alexandre Corthay: Centre for Immune Regulation, Institute of Immunology, University of Oslo and Oslo University Hospital Rikshospitalet, PO Box 4950 Nydalen, 0424 Oslo, Norway.

Nature Communications, 2011, vol. 2, issue 1, 1-12

Abstract: Abstract 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-1α, IL-1β and IL-6) and T helper 1 (Th1)-associated cytokines (interferon-γ (IFN-γ), 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-1β and IL-6 by macrophages. Th1-derived IFN-γ 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.

Date: 2011
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DOI: 10.1038/ncomms1239

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