{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Xu B"],"funding":["U.S. Department of Health & Human Services | NIH | National Institute of Neurological Disorders and Stroke","2021 Exceptional Project Grants from The Breast Cancer Alliance","NIAID NIH HHS","U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases","U.S. Department of Health & Human Services | NIH | National Cancer Institute","NCI NIH HHS","NINDS NIH HHS","California Institute for Regenerative Medicine","V Foundation for Cancer Research","Leukemia and Lymphoma Society"],"pagination":["5908"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8501058"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["12(1)"],"pubmed_abstract":["Oncolytic herpes simplex virus-1 is capable of lysing tumor cells while alerting the immune system. CD47, in collaboration with SIRPα, represents an important immune checkpoint to inhibit phagocytosis by innate immune cells. Here we show locoregional control of glioblastoma by an oncolytic herpes virus expressing a full-length anti(α)-human CD47 IgG1 or IgG4 antibody. The antibodies secreted by the virus-infected glioblastoma cells block the CD47 'don't eat me' signal irrespective of the subclass; however, αCD47-IgG1 has a stronger tumor killing effect than αCD47-IgG4 due to additional antibody-dependent cellular phagocytosis by macrophages and antibody-dependent cellular cytotoxicity by NK cells. Intracranially injected αCD47-IgG1-producing virus continuously releases the respective antib"],"journal":["Nature communications"],"pubmed_title":["An oncolytic virus expressing a full-length antibody enhances antitumor innate immune response to glioblastoma."],"pmcid":["PMC8501058"],"funding_grant_id":["CA163205-01","NS106170","R01 NS106170","P01 CA163205","DISC2COVID19-11947","CA201075","P30 CA033572","R00 CA201075","R01 CA265095","6503-17","R35 CA210087","CA223400","AI129582","R21 CA223400","CA247550","U19 CA264512","R01 CA247550","R01 CA255250","1364-19","CA068458","R01 AI129582","K99 CA201075"],"pubmed_authors":["Tian L","Ma R","Dong W","Antonio Chiocca E","Chen J","Zhang J","Yu J","Wang J","Feng M","Xu B","Li A","Kaur B","Caligiuri MA"],"additional_accession":[]},"is_claimable":false,"name":"An oncolytic virus expressing a full-length antibody enhances antitumor innate immune response to glioblastoma.","description":"Oncolytic herpes simplex virus-1 is capable of lysing tumor cells while alerting the immune system. CD47, in collaboration with SIRPα, represents an important immune checkpoint to inhibit phagocytosis by innate immune cells. Here we show locoregional control of glioblastoma by an oncolytic herpes virus expressing a full-length anti(α)-human CD47 IgG1 or IgG4 antibody. The antibodies secreted by the virus-infected glioblastoma cells block the CD47 'don't eat me' signal irrespective of the subclass; however, αCD47-IgG1 has a stronger tumor killing effect than αCD47-IgG4 due to additional antibody-dependent cellular phagocytosis by macrophages and antibody-dependent cellular cytotoxicity by NK cells. Intracranially injected αCD47-IgG1-producing virus continuously releases the respective antib","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Oct","modification":"2026-03-17T15:19:32.571Z","creation":"2025-04-05T23:59:41.202Z"},"accession":"S-EPMC8501058","cross_references":{"pubmed":["34625564"],"doi":["10.1038/s41467-021-26003-6"]}}