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Cell proliferation and survival induced by toll-like receptors is antagonized by type IIFNs

  1. Author:
    Hasan, U. A.
    Caux, C.
    Perrot, I.
    Doffin, A. C.
    Menetrier-Caux, C.
    Trinchieri, G.
    Tommasino, M.
    Vlach, J.

  2. Author Address

    Int Agcy Res Canc, Infect & Canc Biol Grp, F-69372 Lyon 08, France. Ctr Leon Berard, F-69373 Lyon, France. Innate Pharma, F-69573 Dardilly, France. NCI, Canc & Inflammat Program, Canc Res Ctr, Ft Detrick, MD 21702 USA. Schering Plough Res Inst, Kenilworth, NJ 07033 USA.;Hasan, UA, Int Agcy Res Canc, Infect & Canc Biol Grp, 150 Cours Albert Thomas, F-69372 Lyon 08, France.;hasan@iarc.fr
    1. Year: 2007
    2. Date: May
  2. Journal: Proceedings of the National Academy of Sciences of the United States of America
    1. 104
    2. 19
    3. Pages: 8047-8052
  4. Type of Article: Article
  5. ISSN: 0027-8424
  1. Abstract:

    TRIF is an adaptor protein associated with the signaling by Toll-like receptor (TLR)3 and TLR4 for the induction of type I IFNs. Here, we demonstrate a mechanism by which TLR signaling controls cell proliferation and survival. We show that TLR3 and TLR4 can induce cell cycle entry via TRIF, which targets the cell cycle inhibitor p27(kip1) for relocalization, phosphorylation by cyclin/cdk complexes, and proteasome degradation. These events are antagonized by type I IFN induced by the TRIF pathway. Furthermore, in human dendritic cells treated with TLR3, TLR4, or TLR5 ligands, we demonstrate that IFN signaling modulates p27kipl degradation and apoptosis, identifying an immunoregulatory "switching" function of type I IFNs. These findings reveal a previously uncharacterized function of TLR signaling in cell proliferation and survival.

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External Sources

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  2. DOI: 10.1073/pnas.0700664104
  3. View record in Web of Science®
  4. WOS: 000246461500057

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