TY - JOUR
T1 - Molecular characteristics of immunogenic cancer cell death
AU - Tesniere, A.
AU - Panaretakis, T.
AU - Kepp, O.
AU - Apetoh, L.
AU - Ghiringhelli, F.
AU - Zitvogel, L.
AU - Kroemer, G.
N1 - Funding Information:
Acknowledgements. GK is supported by a special grant from Ligue contre le Cancer (équipe labellisée) as well as by grants from European Commission (Active p53, RIGHT, Trans-Death, Death-Train, ChemoRes) and by Institut National contre le Cancer (INCa). LZ is supported by grants from INCa and from European DC THERA. AT receives a fellowship from Fondation pour la Recherche Medicale. TP receives a fellowship from the Swedish Research Council. LA is supported by Ligue contre le Cancer, and FG by Poste d’Accueil INSERM.
PY - 2008/1/1
Y1 - 2008/1/1
N2 - Apoptotic cell death is initiated by a morphologically homogenous entity that was considered to be non-immunogenic and non-inflammatory in nature. However, recent advances suggest that apoptosis, under certain circumstances, can be immunogenic. In particular, some characteristics of the plasma membrane, acquired at preapoptotic stage, can cause immune effectors to recognize and attack preapoptotic tumor cells. The signals that mediate the immunogenicity of tumor cells involve elements of the DNA damage response (such as ataxia telangiectasia mutated and p53 activation), elements of the endoplasmic reticulum stress response (such as eukaryotic initiation factor 2α phosphorylation), as well as elements of the apoptotic response (such as caspase activation). Depending on the signal-transduction pathway, tumor cells responding to chemotherapy or radiotherapy can express 'danger' and 'eat me' signals on the cell surface (such as NKG2D ligands, heat-shock proteins and calreticulin) or can secrete/release immunostimulatory factors (such as cytokines and high-mobility group box 1) to stimulate innate immune effectors. Likewise, the precise sequence of such events influences the 'decision' of the immune system to mount a cognate response or not. We therefore anticipate that the comprehension of the mechanisms governing the immunogenicity of cell death will have a profound impact on the design of anticancer therapies.
AB - Apoptotic cell death is initiated by a morphologically homogenous entity that was considered to be non-immunogenic and non-inflammatory in nature. However, recent advances suggest that apoptosis, under certain circumstances, can be immunogenic. In particular, some characteristics of the plasma membrane, acquired at preapoptotic stage, can cause immune effectors to recognize and attack preapoptotic tumor cells. The signals that mediate the immunogenicity of tumor cells involve elements of the DNA damage response (such as ataxia telangiectasia mutated and p53 activation), elements of the endoplasmic reticulum stress response (such as eukaryotic initiation factor 2α phosphorylation), as well as elements of the apoptotic response (such as caspase activation). Depending on the signal-transduction pathway, tumor cells responding to chemotherapy or radiotherapy can express 'danger' and 'eat me' signals on the cell surface (such as NKG2D ligands, heat-shock proteins and calreticulin) or can secrete/release immunostimulatory factors (such as cytokines and high-mobility group box 1) to stimulate innate immune effectors. Likewise, the precise sequence of such events influences the 'decision' of the immune system to mount a cognate response or not. We therefore anticipate that the comprehension of the mechanisms governing the immunogenicity of cell death will have a profound impact on the design of anticancer therapies.
UR - http://www.scopus.com/inward/record.url?scp=37349051718&partnerID=8YFLogxK
U2 - 10.1038/sj.cdd.4402269
DO - 10.1038/sj.cdd.4402269
M3 - Review article
C2 - 18007663
AN - SCOPUS:37349051718
SN - 1350-9047
VL - 15
SP - 3
EP - 12
JO - Cell Death and Differentiation
JF - Cell Death and Differentiation
IS - 1
ER -