Fiche publication
Date publication
avril 2007
Auteurs
Membres identifiés du Cancéropôle Est :
Pr GHIRINGHELLI François
Tous les auteurs :
Ghiringhelli F, Apetoh L, Housseau F, Kroemer G, Zitvogel L
Lien Pubmed
Résumé
Cancer results from a tumor cell intrinsic dysregulation of oncogenes, tumor suppressor and stability genes as well as from the avoidance of immunosurveillance. A complex network of cellular interactions allows one to mount cognate anti-tumor immune responses. Recently, discoveries have been made regarding the links between innate and cognate antitumor immunity eliciting protective T-cell responses. The intricate differentiation pathway, whereby dendritic cells can efficiently mature in the tumor microenvironment, appears crucial for the priming of T cells. Transformed cells might deliver danger signals directly to the dendritic cell. Alternatively, other cell types belonging to the innate immune system can sense transformed cells through a specific set of receptors and then interact with dendritic cells to modulate their activation state. A novel subset of innate effector cells called interferon-producing killer dendritic cells are multitasking chimeras that can recognize and kill transformed cells, and undergo a maturation state of antigen presentation. Also, evidence has been produced suggesting that cell death promoted by conventional chemotherapy or radiotherapy might elicit interactions between the innate and the cognate immune system that result in anti-tumor immune responses.
Référence
Curr Opin Immunol. 2007 Apr;19(2):224-31
