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IL-6-mediated environmental conditioning of defective Th1 differentiation dampens antitumour immune responses in old age

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  • Hirotake Tsukamoto

    (Graduate School of Medical Sciences, Kumamoto University)

  • Satoru Senju

    (Graduate School of Medical Sciences, Kumamoto University)

  • Keiko Matsumura

    (Graduate School of Medical Sciences, Kumamoto University)

  • Susan L. Swain

    (University of Massachusetts Medical School)

  • Yasuharu Nishimura

    (Graduate School of Medical Sciences, Kumamoto University)

Abstract

Decline in immune function and inflammation concomitantly develop with ageing. Here we focus on the impact of this inflammatory environment on T cells, and demonstrate that in contrast to successful tumour elimination in young mice, replenishment of tumour-specific CD4+ T cells fails to induce tumour regression in aged hosts. The impaired antitumour effect of CD4+ T cells with their defective Th1 differentiation in an aged environment is restored by interleukin (IL)-6 blockade or IL-6 deficiency. IL-6 blockade also restores the impaired ability of CD4+ T cells to promote CD8+ T-cell-dependent tumour elimination in aged mice, which requires IFN-γ. Furthermore, IL-6-stimulated production of IL-4/IL-21 through c-Maf induction is responsible for impaired Th1 differentiation. IL-6 also contributes to IL-10 production from CD4+ T cells in aged mice, causing attenuated responses of CD8+ T cells. These findings suggest that IL-6 serves as an extrinsic factor counteracting CD4+ T-cell-mediated immunity against tumour in old age.

Suggested Citation

  • Hirotake Tsukamoto & Satoru Senju & Keiko Matsumura & Susan L. Swain & Yasuharu Nishimura, 2015. "IL-6-mediated environmental conditioning of defective Th1 differentiation dampens antitumour immune responses in old age," Nature Communications, Nature, vol. 6(1), pages 1-15, November.
  • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms7702
    DOI: 10.1038/ncomms7702
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