Autophagy-dependent suppression of cancer immunogenicity and effector mechanisms of innate and adaptive immunity.
Autophagy-dependent suppression of cancer immunogenicity and effector mechanisms of innate and adaptive immunity.
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DOI：
10.4161/onci.26260
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发表时间：
2013-10-01
期刊：
影响因子：
7.2
通讯作者：
Agostinis P
中科院分区：
文献类型：
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作者：
Garg AD;Dudek AM;Agostinis P
对自噬调节免疫原性细胞死亡的机制的研究表明，癌细胞对依赖于活性氧的内质网应激的自噬反应抑制了细胞表面钙网蛋白的暴露，抑制了树突状细胞(DC)的表型成熟及其释放IL-6的能力，并支持(产生干扰素γ的)CD_4~+和CD_8~+T淋巴细胞的增殖。这些发现揭示了治疗诱导的自噬在抑制免疫原性细胞死亡所引发的抗癌免疫反应的关键机制方面所发挥的前所未有的作用。
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.