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Host STING-dependent MDSC mobilization drives extrinsic radiation resistance.

Abstract：

:Radiotherapy induces and promotes innate and adaptive immunity in which host STING plays an important role. However, radioresistance in irradiated tumors can also develop, resulting in relapse. Here we report a mechanism by which extrinsic resistance develops after local ablative radiation that relies on the immunosuppressive action of STING. The STING/type I interferon pathway enhances suppressive inflammation in tumors by recruiting myeloid cells in part via the CCR2 pathway. Germ-line knockouts of CCR2 or treatment with an anti-CCR2 antibody results in blockade of radiation-induced MDSC infiltration. Treatment with anti-CCR2 antibody alleviates immunosuppression following activation of the STING pathway, enhancing the anti-tumor effects of STING agonists and radiotherapy. We propose that radiation-induced STING activation is immunosuppressive due to (monocytic) M-MDSC infiltration, which results in tumor radioresistance. Furthermore, the immunosuppressive effects of radiotherapy and STING agonists can be abrogated in humans by a translational strategy involving anti-CCR2 antibody treatment to improve radiotherapy.

journal_name

Nat Commun

journal_title

Nature communications

authors

Liang H,Deng L,Hou Y,Meng X,Huang X,Rao E,Zheng W,Mauceri H,Mack M,Xu M,Fu YX,Weichselbaum RR

doi

10.1038/s41467-017-01566-5

subject

Has Abstract

pub_date

2017-11-23 00:00:00

pages

1736

issue

1

issn

2041-1723

pii

10.1038/s41467-017-01566-5

journal_volume

8

pub_type

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