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. 2021 Jul 6;81(10):1128–1144. doi: 10.1055/a-1475-4335

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The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution-NonDerivative-NonCommercial License, permitting copying and reproduction so long as the original work is given appropriate credit. Contents may not be used for commecial purposes, or adapted, remixed, transformed or built upon. ( https://creativecommons.org/licenses/by-nc-nd/4.0/ )

This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License, which permits unrestricted reproduction and distribution, for non-commercial purposes only; and use and reproduction, but not distribution, of adapted material for non-commercial purposes only, provided the original work is properly cited.

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Fig. 2 — PARPi-mediated tumour cell effects allowing combined treatment with immune checkpoint blockade. PARP inhibition (similar to BRCA1/2 loss of function) leads to an accumulation of fragmented double-stranded DNA (dsDNA) in the cytosol of the tumour cell. This activates the cGAS/STING signalling pathway, which ultimately triggers a type I interferon response. This also releases downstream chemokines (CXCL10, CXCL11, CCL5), among others, which attract tumour-suppressive T and NK cells into the tumour. However, PD-L1 expression is also upregulated in the tumour microenvironment. Both immune cell recruitment and PD-L1 induction now permit effective immune checkpoint blockade.