{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Liu D"],"funding":["NCATS NIH HHS","NHLBI NIH HHS","National Heart, Lung, and Blood Institute","American Society of Hematology"],"pagination":["3243-3252"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6785373"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["59(10)"],"pubmed_abstract":["<h4>Background</h4>Only a fraction of red blood cell (RBC) transfusion recipients form alloantibodies, and variables determining responsiveness or nonresponsiveness are poorly understood. We and others have previously shown in animal models that pretreatment with toll-like receptor agonists that mimic different types of infections impacts the magnitude or frequency of RBC alloantibody responses. We hypothesized that influenza infection, coexistent with transfusion, would impact responses to transfused RBCs in a manner dependent on Type 1(α/β) interferon (IFN) signaling and tested this in a murine model.<h4>Study design and methods</h4>Wild-type mice or mice lacking the ability to respond to Type 1 IFN were infected with influenza prior to the transfusion of transgenic murine RBCs (K1) expr"],"journal":["Transfusion"],"pubmed_title":["Type 1 IFN signaling critically regulates influenza-induced alloimmunization to transfused KEL RBCs in a murine model."],"pmcid":["PMC6785373"],"funding_grant_id":["R01 HL132951","R01 HL126076","K08HL141446","K08 HL141446","HL132951","HL126076","UL1 TR001863","Scholar Award"],"pubmed_authors":["Xu L","Liu J","Eisenbarth SC","Gibb DR","Hendrickson JE","Santhanakrishnan M","Liu D","Shi Z","Escamilla-Rivera V"],"additional_accession":[]},"is_claimable":false,"name":"Type 1 IFN signaling critically regulates influenza-induced alloimmunization to transfused KEL RBCs in a murine model.","description":"<h4>Background</h4>Only a fraction of red blood cell (RBC) transfusion recipients form alloantibodies, and variables determining responsiveness or nonresponsiveness are poorly understood. We and others have previously shown in animal models that pretreatment with toll-like receptor agonists that mimic different types of infections impacts the magnitude or frequency of RBC alloantibody responses. We hypothesized that influenza infection, coexistent with transfusion, would impact responses to transfused RBCs in a manner dependent on Type 1(α/β) interferon (IFN) signaling and tested this in a murine model.<h4>Study design and methods</h4>Wild-type mice or mice lacking the ability to respond to Type 1 IFN were infected with influenza prior to the transfusion of transgenic murine RBCs (K1) expr","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 Oct","modification":"2025-04-05T23:38:18.201Z","creation":"2020-10-08T07:17:46Z"},"accession":"S-EPMC6785373","cross_references":{"pubmed":["31403208"],"doi":["10.1111/trf.15482"]}}