TY - JOUR
T1 - Killer dendritic cells
T2 - IKDC and the others
AU - Bonmort, Mathieu
AU - Dalod, Marc
AU - Mignot, Grégoire
AU - Ullrich, Evelyn
AU - Chaput, Nathalie
AU - Zitvogel, Laurence
N1 - Funding Information:
We thank Régis Josien and Franck Housseau for careful reading and helpful discussions. M Bonmort was supported by a Poste d’Accueil INSERM, G Mignot by the Association pour la Recherche sur le Cancer, and E Ullrich received a fellowship from the German Forschungsgemeinschaft (DFG) and Fondation pour la Recherche Médicale (FRM). L Zitvogel received a grant from INCa, Cancéropôle Idf and LIGUE labelisée contre le Cancer.
PY - 2008/10/1
Y1 - 2008/10/1
N2 - Tumors can regress as a result of invading myeloid and lymphoid cells that act in concert. Although the myeloid cells are widely recognized as antigen presenters and lymphoid cells as classical effectors, recent evidence revealed the capacity of dendritic cells (DC) to kill tumor cells. The functional concept of 'natural killer (NK) myeloid DC' is supported by mouse and human in vitro data that may be clinically relevant because human killer DC can contribute to tumor shrinking during topical therapy with toll-like receptor (TLR) agonists. Whether tumor killing by DC is a 'catalyzing' step for efficient crosspresentation and/or a promoting step for an immunogenic cell death pathway remains an open question. We also discuss how interferon-producing killer DC (IKDC) may participate in the control of tumor progression.
AB - Tumors can regress as a result of invading myeloid and lymphoid cells that act in concert. Although the myeloid cells are widely recognized as antigen presenters and lymphoid cells as classical effectors, recent evidence revealed the capacity of dendritic cells (DC) to kill tumor cells. The functional concept of 'natural killer (NK) myeloid DC' is supported by mouse and human in vitro data that may be clinically relevant because human killer DC can contribute to tumor shrinking during topical therapy with toll-like receptor (TLR) agonists. Whether tumor killing by DC is a 'catalyzing' step for efficient crosspresentation and/or a promoting step for an immunogenic cell death pathway remains an open question. We also discuss how interferon-producing killer DC (IKDC) may participate in the control of tumor progression.
UR - http://www.scopus.com/inward/record.url?scp=50549099693&partnerID=8YFLogxK
U2 - 10.1016/j.coi.2008.04.006
DO - 10.1016/j.coi.2008.04.006
M3 - Review article
C2 - 18554881
AN - SCOPUS:50549099693
SN - 0952-7915
VL - 20
SP - 558
EP - 565
JO - Current Opinion in Immunology
JF - Current Opinion in Immunology
IS - 5
ER -