TY - JOUR
T1 - Autophagy, Inflammation, and Immunity
T2 - A Troika Governing Cancer and Its Treatment
AU - Zhong, Zhenyu
AU - Sanchez-Lopez, Elsa
AU - Karin, Michael
N1 - Publisher Copyright:
© 2016 Elsevier Inc.
PY - 2016/7/14
Y1 - 2016/7/14
N2 - Autophagy, a cellular waste disposal process, has well-established tumor-suppressive properties. New studies indicate that, in addition to its cell-autonomous anti-tumorigenic functions, autophagy inhibits cancer development by orchestrating inflammation and immunity. While attenuating tumor-promoting inflammation, autophagy enhances the processing and presentation of tumor antigens and thereby stimulates anti-tumor immunity. Although cancer cells can escape immunosurveillance by tuning down autophagy, certain chemotherapeutic agents with immunogenic properties may enhance anti-tumor immunity by inducing autophagic cell death. Understanding the intricate and complex relationships within this troika and how they are affected by autophagy enhancing drugs should improve the efficacy of cancer immunotherapy.
AB - Autophagy, a cellular waste disposal process, has well-established tumor-suppressive properties. New studies indicate that, in addition to its cell-autonomous anti-tumorigenic functions, autophagy inhibits cancer development by orchestrating inflammation and immunity. While attenuating tumor-promoting inflammation, autophagy enhances the processing and presentation of tumor antigens and thereby stimulates anti-tumor immunity. Although cancer cells can escape immunosurveillance by tuning down autophagy, certain chemotherapeutic agents with immunogenic properties may enhance anti-tumor immunity by inducing autophagic cell death. Understanding the intricate and complex relationships within this troika and how they are affected by autophagy enhancing drugs should improve the efficacy of cancer immunotherapy.
UR - http://www.scopus.com/inward/record.url?scp=84978197362&partnerID=8YFLogxK
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U2 - 10.1016/j.cell.2016.05.051
DO - 10.1016/j.cell.2016.05.051
M3 - Review article
C2 - 27419869
AN - SCOPUS:84978197362
SN - 0092-8674
VL - 166
SP - 288
EP - 298
JO - Cell
JF - Cell
IS - 2
ER -