{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Hsieh RC"],"funding":["NCI NIH HHS"],"pagination":["eabl9330"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9373855"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["7(72)"],"pubmed_abstract":["Radiotherapy (RT) of colorectal cancer (CRC) can prime adaptive immunity against tumor-associated antigen (TAA)-expressing CRC cells systemically. However, abscopal tumor remissions are extremely rare, and the postirradiation immune escape mechanisms in CRC remain elusive. Here, we found that irradiated CRC cells used ATR-mediated DNA repair signaling pathway to up-regulate both CD47 and PD-L1, which through engagement of SIRPα and PD-1, respectively, prevented phagocytosis by antigen-presenting cells and thereby limited TAA cross-presentation and innate immune activation. This postirradiation CD47 and PD-L1 up-regulation was observed across various human solid tumor cells. Concordantly, rectal cancer patients with poor responses to neoadjuvant RT exhibited significantly elevated postirrad"],"journal":["Science immunology"],"pubmed_title":["ATR-mediated CD47 and PD-L1 up-regulation restricts radiotherapy-induced immune priming and abscopal responses in colorectal cancer."],"pmcid":["PMC9373855"],"funding_grant_id":["P30 CA016672","R01 CA231360"],"pubmed_authors":["Prasad R","Kim YSB","De Azevedo RA","Jayaprakash P","Lin SH","Srinivasamani A","Chou YC","Boda AR","Rudqvist NP","Bhanu KR","Venkatesulu BP","DePinho RA","Hsieh RC","Morrow B","Taniguchi C","Hsu WH","Slay R","Chen J","Chan LC","Hartley G","Vilar E","Wu RC","Chen CH","Krishnan S","Gubin M","Hegde SM","Winkler M","Hung MC","Lea ST","Liu A","Steiner M","Couillault CA","Wang CC","Curran MA"],"additional_accession":[]},"is_claimable":false,"name":"ATR-mediated CD47 and PD-L1 up-regulation restricts radiotherapy-induced immune priming and abscopal responses in colorectal cancer.","description":"Radiotherapy (RT) of colorectal cancer (CRC) can prime adaptive immunity against tumor-associated antigen (TAA)-expressing CRC cells systemically. However, abscopal tumor remissions are extremely rare, and the postirradiation immune escape mechanisms in CRC remain elusive. Here, we found that irradiated CRC cells used ATR-mediated DNA repair signaling pathway to up-regulate both CD47 and PD-L1, which through engagement of SIRPα and PD-1, respectively, prevented phagocytosis by antigen-presenting cells and thereby limited TAA cross-presentation and innate immune activation. This postirradiation CD47 and PD-L1 up-regulation was observed across various human solid tumor cells. Concordantly, rectal cancer patients with poor responses to neoadjuvant RT exhibited significantly elevated postirrad","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Jun","modification":"2025-04-21T22:26:37.998Z","creation":"2025-04-05T18:45:15.584Z"},"accession":"S-EPMC9373855","cross_references":{"pubmed":["35687697"],"doi":["10.1126/sciimmunol.abl9330"]}}