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

Author

Listed:
  • 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.
    University of Oslo, PO Box 1041 Blindern, 0316 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.)

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.

Suggested Citation

  • Ole Audun Werner Haabeth & Kristina Berg Lorvik & Clara Hammarström & Ian M. Donaldson & Guttorm Haraldsen & Bjarne Bogen & Alexandre Corthay, 2011. "Inflammation driven by tumour-specific Th1 cells protects against B-cell cancer," Nature Communications, Nature, vol. 2(1), pages 1-12, September.
    • Handle: RePEc:nat:natcom:v:2:y:2011:i:1:d:10.1038_ncomms1239
    DOI: 10.1038/ncomms1239
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