Abstract
The inspection of the mechanisms through which autophagy modulates immunogenic cell death revealed that the autophagic response of cancer cells to reactive oxygen species-dependent endoplasmic reticulum stress suppresses the exposure of calreticulin on the cell surface, the phenotypic maturation of dendritic cells (DCs) as well as their ability to release interleukin-6 and to support the proliferative expansion of (interferon γ-producing) CD4(+) and CD8(+) T lymphocytes. These findings unveil an unprecedented role for therapy-induced autophagy in suppressing key mechanisms that underlie anticancer immune responses as elicited by immunogenic cell death.