{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Gibb DR"],"funding":["NCATS NIH HHS","NHLBI NIH HHS","National Blood Foundation","National Institutes of Health"],"pagination":["2595-2608"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5745367"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["57(11)"],"pubmed_abstract":["<h4>Background</h4>Alloantibodies to red blood cell (RBC) antigens can cause significant hemolytic events. Prior studies have demonstrated that inflammatory stimuli in animal models and inflammatory states in humans, including autoimmunity and viremia, promote alloimmunization. However, molecular mechanisms underlying these findings are poorly understood. Given that Type 1 interferons (IFN-α/β) regulate antiviral immunity and autoimmune pathology, the hypothesis that IFN-α/β regulates RBC alloimmunization was tested in a murine model.<h4>Study design and methods</h4>Leukoreduced murine RBCs expressing the human KEL glycoprotein were transfused into control mice (WT), mice lacking the unique IFN-α/β receptor (IFNAR1<sup>-/-</sup> ), or bone marrow chimeric mice lacking IFNAR1 on specific ce"],"journal":["Transfusion"],"pubmed_title":["B cells require Type 1 interferon to produce alloantibodies to transfused KEL-expressing red blood cells in mice."],"pmcid":["PMC5745367"],"funding_grant_id":["R01 HL126076","T32 HL007974","R13672","T32 HL007974‐14","UL1 TR001863"],"pubmed_authors":["Tormey CA","Liu J","Iwasaki A","Eisenbarth SC","Gibb DR","Stowell SR","Hendrickson JE","Santhanakrishnan M","Patel S","Madrid DJ","Natarajan P"],"additional_accession":[]},"is_claimable":false,"name":"B cells require Type 1 interferon to produce alloantibodies to transfused KEL-expressing red blood cells in mice.","description":"<h4>Background</h4>Alloantibodies to red blood cell (RBC) antigens can cause significant hemolytic events. Prior studies have demonstrated that inflammatory stimuli in animal models and inflammatory states in humans, including autoimmunity and viremia, promote alloimmunization. However, molecular mechanisms underlying these findings are poorly understood. Given that Type 1 interferons (IFN-α/β) regulate antiviral immunity and autoimmune pathology, the hypothesis that IFN-α/β regulates RBC alloimmunization was tested in a murine model.<h4>Study design and methods</h4>Leukoreduced murine RBCs expressing the human KEL glycoprotein were transfused into control mice (WT), mice lacking the unique IFN-α/β receptor (IFNAR1<sup>-/-</sup> ), or bone marrow chimeric mice lacking IFNAR1 on specific ce","dates":{"release":"2017-01-01T00:00:00Z","publication":"2017 Nov","modification":"2025-04-04T01:54:48.947Z","creation":"2019-03-27T00:04:55Z"},"accession":"S-EPMC5745367","cross_references":{"pubmed":["28836263"],"doi":["10.1111/trf.14288"]}}