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Comment
. 2012 Mar 7;31(5):1055-7.
doi: 10.1038/emboj.2012.2. Epub 2012 Jan 17.

Enlightening the impact of immunogenic cell death in photodynamic cancer therapy

Lorenzo Galluzzi  1 , Oliver Kepp, Guido Kroemer
Affiliations
Comment

Enlightening the impact of immunogenic cell death in photodynamic cancer therapy

Lorenzo Galluzzi et al. EMBO J. .

Abstract

EMBO J 31 5, 1062–1079 (2012); published online January 17 2012

In this issue of The EMBO Journal, Garg et al (2012) delineate a signalling pathway that leads to calreticulin (CRT) exposure and ATP release by cancer cells that succumb to photodynamic therapy (PTD), thereby providing fresh insights into the molecular regulation of immunogenic cell death (ICD).

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Conflict of interest statement

The authors declare that they have no conflict of interest.

Figures

Figure 1
Figure 1
Molecular mechanisms of immunogenic cell death (ICD). At least three processes underlie the immunogenicity of cell death: the pre-apoptotic exposure of calreticulin (CRT) at the cell surface, the secretion of ATP, and the post-apoptotic release of HMGB1. ICD can be triggered by multiple stimuli, including photodynamic therapy, anthracycline-based chemotherapy, and some types of radiotherapy. The signalling pathways elicited by distinct ICD inducers overlap, but are not identical. In red are indicated molecules and processes that—according to current knowledge—may be required for CRT exposure and ATP secretion in response to most, if not all, ICD inducers. The molecular determinants of the immunogenic release of HMGB1 remain poorly understood. ER, endoplasmic reticulum; P-eIF2α, phosphorylated eIF2α; PI3K, class I phosphoinositide-3-kinase; ROS, reactive oxygen species.
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