Tumor promotion by intratumoral plasmacytoid dendritic cells is reversed by TLR7 ligand treatment.

نویسندگان

  • Isabelle Le Mercier
  • Dominique Poujol
  • Amélien Sanlaville
  • Vanja Sisirak
  • Michael Gobert
  • Isabelle Durand
  • Bertrand Dubois
  • Isabelle Treilleux
  • Jacqueline Marvel
  • Jaromir Vlach
  • Jean-Yves Blay
  • Nathalie Bendriss-Vermare
  • Christophe Caux
  • Isabelle Puisieux
  • Nadège Goutagny
چکیده

Plasmacytoid dendritic cells (pDC) are key regulators of antiviral immunity. In previous studies, we reported that pDC-infiltrating human primary breast tumors represent an independent prognostic factor associated with poor outcome. To understand this negative impact of tumor-associated pDC (TApDC), we developed an orthotopic murine mammary tumor model that closely mimics the human pathology, including pDC and regulatory T cell (Treg) infiltration. We showed that TApDC are mostly immature and maintain their ability to internalize antigens in vivo and to activate CD4(+) T cells. Most importantly, TApDC were specifically altered for cytokine production in response to Toll-like receptor (TLR)-9 ligands in vitro while preserving unaltered response to TLR7 ligands (TLR7L). In vivo pDC depletion delayed tumor growth, showing that TApDC provide an immune-subversive environment, most likely through Treg activation, thus favoring tumor progression. However, in vivo intratumoral administration of TLR7L led to TApDC activation and displayed a potent curative effect. Depletion of pDC and type I IFN neutralization prevented TLR7L antitumoral effect. Our results establish a direct contribution of TApDC to primary breast tumor progression and rationalize the application of TLR7 ligands to restore TApDC activation in breast cancer. Cancer Res; 73(15); 4629-40. ©2013 AACR.

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عنوان ژورنال:
  • Cancer research

دوره 73 15  شماره 

صفحات  -

تاریخ انتشار 2013