Locher, C. (Clara)

Filtering

20111

Settings

Author search.filters.isAuthorOfPublication.1e07ae15-be40-4c19-a29a-2b1cd5c562a4

Search Results

Now showing 1 - 1 of 1
  • Thumbnail Image
    Contribution of IL-17-producing gamma delta T cells to the efficacy of anticancer chemotherapy
    (Rockefeller University Press, 2011) Delahaye, N.F. (Nicolas F.); Ghiringhelli, F. (François); Chaput, N. (Nathalie); Mattarollo, S.R. (Stephen R.); Tesniere, A. (Antoine); Ikuta, K. (Koichi); Kroemer, G. (Guido); Ryffel, B. (Bernard); Pereira, P. (Pablo); Casares, N. (Noelia); Matsuzaki, G. (Goro); Benlagha, K. (Kamel); Apetoh, L. (Lionel); Smyth, M.J. (Mark J.); Zitvogel, L. (Laurence); Ma, Y. (Yuting); Dechanet-Mervill, J. (Julie); Boucontet, L. (Laurent); Ibrahim, N. (Nicolás); Locher, C. (Clara); Aymeric, L. (Laetitia); Lasarte, J.J. (Juan José)
    By triggering immunogenic cell death, some anticancer compounds, including anthracyclines and oxaliplatin, elicit tumor-specific, interferon-γ-producing CD8(+) αβ T lymphocytes (Tc1 CTLs) that are pivotal for an optimal therapeutic outcome. Here, we demonstrate that chemotherapy induces a rapid and prominent invasion of interleukin (IL)-17-producing γδ (Vγ4(+) and Vγ6(+)) T lymphocytes (γδ T17 cells) that precedes the accumulation of Tc1 CTLs within the tumor bed. In T cell receptor δ(-/-) or Vγ4/6(-/-) mice, the therapeutic efficacy of chemotherapy was compromised, no IL-17 was produced by tumor-infiltrating T cells, and Tc1 CTLs failed to invade the tumor after treatment. Although γδ T17 cells could produce both IL-17A and IL-22, the absence of a functional IL-17A-IL-17R pathway significantly reduced tumor-specific T cell responses elicited by tumor cell death, and the efficacy of chemotherapy in four independent transplantable tumor models. Adoptive transfer of γδ T cells restored the efficacy of chemotherapy in IL-17A(-/-) hosts. The anticancer effect of infused γδ T cells was lost when they lacked either IL-1R1 or IL-17A. Conventional helper CD4(+) αβ T cells failed to produce IL-17 after chemotherapy. We conclude that γδ T17 cells play a decisive role in chemotherapy-induced anticancer immune responses.