{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Panda AK"],"funding":["Division of Intramural Research (DIR, NIAID)","Intramural NIH HHS","Division of Intramural Research"],"pagination":["1938-1955"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12560147"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["13(12)"],"pubmed_abstract":["Immune checkpoint blockade for the treatment of malignancies has been focused on reversing inhibitory pathways in T lymphocytes. NK cells are a potent innate defense against tumors and virally infected cells, but their therapeutic manipulation for anticancer immunity has been inadequately explored. Considerable attention has been focused on approaches to blocking inhibitory receptors on NK and myeloid cells. Most effort has been directed to the killer immunoglobulin-like receptors and CD94/NKG2A on NK cells. Another set of receptors with similar function in both NK cells and myeloid cells is the leukocyte immunoglobulin-like receptors (LILR) that interact with a wide variety of HLA molecules. Using pan-anti-HLA mAbs that recognize a conserved epitopic region on HLA also seen by LILRs, we i"],"journal":["Cancer immunology research"],"pubmed_title":["Antibody-Mediated Inhibition of HLA/LILR Interactions Breaks Innate Immune Tolerance and Induces Antitumor Immunity."],"pmcid":["PMC12560147"],"funding_grant_id":["1ZIAAI000224-40","ZIA AI000224"],"pubmed_authors":["Jiang J","Margulies DH","Buszko M","Hernandez JM","Chempati S","Panda AK","Fisk B","Desai PP","Kazmi S","Larrain CM","Remmert K","Blakely AM","Douagi I","Shevach EM","Sinha S","Natarajan K","Kim YH","Teke ME","Boyd LF"],"additional_accession":[]},"is_claimable":false,"name":"Antibody-Mediated Inhibition of HLA/LILR Interactions Breaks Innate Immune Tolerance and Induces Antitumor Immunity.","description":"Immune checkpoint blockade for the treatment of malignancies has been focused on reversing inhibitory pathways in T lymphocytes. NK cells are a potent innate defense against tumors and virally infected cells, but their therapeutic manipulation for anticancer immunity has been inadequately explored. Considerable attention has been focused on approaches to blocking inhibitory receptors on NK and myeloid cells. Most effort has been directed to the killer immunoglobulin-like receptors and CD94/NKG2A on NK cells. Another set of receptors with similar function in both NK cells and myeloid cells is the leukocyte immunoglobulin-like receptors (LILR) that interact with a wide variety of HLA molecules. Using pan-anti-HLA mAbs that recognize a conserved epitopic region on HLA also seen by LILRs, we i","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Dec","modification":"2026-07-15T13:31:08.877Z","creation":"2026-07-05T03:08:28.227Z"},"accession":"S-EPMC12560147","cross_references":{"pubmed":["41032026"],"doi":["10.1158/2326-6066.CIR-25-0343"]}}