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Plasmacytoid dendritic cells mediate oral tolerance

  1. Author:
    Goubier, A.
    Dubois, B.
    Gheit, H.
    Joubert, G.
    Villard-Truc, F.
    Asselin-Paturel, C.
    Trinchieri, G.
    Kaiserlian, D.

  2. Author Address

    Goubier, Anne, Dubois, Bertrand, Gheit, Hanane, Joubert, Grgoire, Kaiserlian, Dominique] INSERM, U851, F-69007 Lyon, France. [Goubier, Anne, Dubois, Bertrand, Gheit, Hanane, Joubert, Grgoire, Kaiserlian, Dominique] Univ Lyon 1, IFR128, F-69622 Villeurbanne, France. [Villard-Truc, Florence] Hop Edouard Herriot, Hosp Civils Lyon, Serv Gastroenterol Pediat, F-69003 Lyon, France. [Asselin-Paturel, Carine, Trinchieri, Giorgio] Schering Plough Lab Immunol Res, F-69570 Dardilly, France. [Trinchieri, Giorgio] NCI, Ctr Canc Res, Canc & Inflammat Program, Frederick, MD 21702 USA.
    1. Year: 2008
  2. Journal: Immunity
    1. 29
    2. 3
    3. Pages: 464-475
  4. Type of Article: Article
  1. Abstract:

    Oral tolerance prevents oral sensitization to dietary antigens (Ags), including proteins and haptens, and development of delayed-type hypersensitivity (DTH) responses. We showed here that plasmacytoid dendritic cells (pDCs) prevented oral T cell priming and were responsible for systemic tolerance to CD4(+) and CD8(+) T cell-mediated DTH responses induced by Ag feeding. Systemic depletion of pDCs prevented induction of tolerance by antigen feeding. Transfer of oral Ag-loaded liver pDCs to naive recipient mice induced Ag-specific suppression of CD4(+) and CD8(+) T cell responses to protein and hapten, respectively. Liver is a site of oral Ag presentation, and pDCs appeared to induce anergy or deletion of Ag-specific T cells in the liver relatively rapidly via a CD4(+) T cell-independent mechanism. These data demonstrate that oral tolerance relies on Ag presentation by pDC to T cells and suggest that pDC could represent a key therapeutic target for intestinal and systemic inflammatory diseases.

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External Sources

  1. PMID: 18789731

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