Oncotarget

Reviews:

Autophagy-associated immune responses and cancer immunotherapy

Hongming Pan, Liuxi Chen, Yinghua Xu, Weidong Han, Fang Lou, Weiqiang Fei, Shuiping Liu, Zhao Jing and Xinbing Sui _

PDF  |  HTML  |  How to cite

Oncotarget. 2016; 7:21235-21246. https://doi.org/10.18632/oncotarget.6908

Metrics: PDF 3786 views  |   HTML 4226 views  |   ?  


Abstract

Hongming Pan1,2,*, Liuxi Chen1,2,*, Yinghua Xu1,2, Weidong Han1,2, Fang Lou1,2, Weiqiang Fei2, Shuiping Liu2, Zhao Jing2 and Xinbing Sui1,2

1 Department of Medical Oncology, Sir Run Run Shaw Hospital, Zhejiang University, Hangzhou, China

2 Biomedical Research Center and Key Laboratory of Biotherapy of Zhejiang Province, Hangzhou, China

* These authors have contributed equally to this work

Correspondence to:

Xinbing Sui, email:

Keywords: autophagy, immune, cancer immunotherapy

Received: September 16, 2015 Accepted: January 06, 2016 Published: January 13, 2016

Abstract

Autophagy is an evolutionarily conserved catabolic process by which cellular components are sequestered into a double-membrane vesicle and delivered to the lysosome for terminal degradation and recycling. Accumulating evidence suggests that autophagy plays a critical role in cell survival, senescence and homeostasis, and its dysregulation is associated with a variety of diseases including cancer, cardiovascular disease, neurodegeneration. Recent studies show that autophagy is also an important regulator of cell immune response. However, the mechanism by which autophagy regulates tumor immune responses remains elusive. In this review, we will describe the role of autophagy in immune regulation and summarize the possible molecular mechanisms that are currently well documented in the ability of autophagy to control cell immune response. In addition, the scientific and clinical hurdles regarding the potential role of autophagy in cancer immunotherapy will be discussed.


Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 6908