Targeting immunogenic cell death in cancer

Molecular Oncology - Tập 14 Số 12 - Trang 2994-3006 - 2020
Asma Ahmed1,2, Stephen W. G. Tait1,2
1Cancer Research UK Beatson Institute, Glasgow, UK
2Institute of Cancer Sciences, University of Glasgow, UK

Tóm tắt

Immunogenic cell death (ICD) is a type of cancer cell death triggered by certain chemotherapeutic drugs, oncolytic viruses, physicochemical therapies, photodynamic therapy, and radiotherapy. It involves the activation of the immune system against cancer in immunocompetent hosts. ICD comprises the release of damage‐associated molecular patterns (DAMPs) from dying tumor cells that result in the activation of tumor‐specific immune responses, thus eliciting long‐term efficacy of anticancer drugs by combining direct cancer cell killing and antitumor immunity. Remarkably, subcutaneous injection of dying tumor cells undergoing ICD has been shown to provoke anticancer vaccine effects in vivo. DAMPs include the cell surface exposure of calreticulin (CRT) and heat‐shock proteins (HSP70 and HSP90), extracellular release of adenosine triphosphate (ATP), high‐mobility group box‐1 (HMGB1), type I IFNs and members of the IL‐1 cytokine family. In this review, we discuss the cell death modalities connected to ICD, the DAMPs exposed during ICD, and the mechanism by which they activate the immune system. Finally, we discuss the therapeutic potential and challenges of harnessing ICD in cancer immunotherapy.

Từ khóa


Tài liệu tham khảo

10.1038/s41418-017-0012-4

10.3389/fimmu.2015.00588

10.1016/j.molcel.2019.09.006

10.1126/science.1071059

10.1038/nrc3380

10.1038/nri.2017.9

10.1038/nrm3722

10.1038/ni.3253

10.1038/35037722

10.1038/nrm2312

10.1038/s41580-019-0173-8

10.1098/rsob.180002

10.1016/j.molmed.2017.11.002

10.1038/ncb3596

10.1016/j.devcel.2013.11.015

10.1016/j.cell.2014.11.037

10.1016/j.cell.2014.11.036

10.1016/j.molcel.2019.02.013

10.1016/j.immuni.2008.05.013

10.1038/s41590-020-0641-5

10.1038/s41418-018-0214-4

10.1158/0008-5472.CAN-11-0950

10.1007/s00262-011-1184-2

10.1038/nm1523

10.1038/cdd.2017.65

10.1038/nrm.2016.149

10.1016/j.celrep.2016.03.037

10.1056/NEJMra1310050

10.1126/sciimmunol.aaw2004

10.1126/science.aad0395

10.1038/s41577-019-0228-2

10.1038/s41586-019-1770-6

10.1038/nature15514

10.1126/science.aau2818

10.1038/ncomms14128

10.1038/nature22393

10.1038/s41586-020-2071-9

10.1038/s41586-020-2079-1

10.1038/s41467-019-09397-2

10.1111/imr.12287

10.1016/j.immuni.2017.11.013

10.1038/emboj.2011.497

10.1038/nm.2028

10.1111/febs.13775

10.1038/nm.3708

10.15252/embr.201949799

10.1080/2162402X.2019.1655964

10.1186/s40425-019-0550-z

10.1146/annurev-immunol-032712-100008

10.1038/nm1622

10.2119/molmed.2011.00389

10.1038/ni.2376

10.1016/j.canlet.2015.07.008

10.1111/j.1582-4934.2008.00273.x

10.1038/nm0598-581

10.1038/onc.2015.82

10.1371/journal.pone.0031732

10.1038/onc.2010.500

10.1038/s41586-019-1593-5

10.1016/j.immuni.2017.07.016

10.1016/j.molcel.2014.03.040

10.1016/S1359-6101(01)00022-3

10.1038/ni1213

10.4049/jimmunol.1004163

10.1016/j.immuni.2014.10.019