{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Escamilla-Rivera V"],"funding":["NCATS NIH HHS","NHLBI NIH HHS"],"pagination":["1983-1993"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7256361"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["135(22)"],"pubmed_abstract":["Polyclonal anti-D (Rh immune globulin [RhIg]) therapy has mitigated hemolytic disease of the newborn over the past half century, although breakthrough anti-D alloimmunization still occurs in some treated females. We hypothesized that antiviral responses may impact the efficacy of immunoprophylaxis therapy in a type 1 interferon (IFN)-dependent manner and tested this hypothesis in a murine model of KEL alloimmunization. Polyclonal anti-KEL immunoprophylaxis (KELIg) was administered to wild-type or knockout mice in the presence or absence of polyinosinic-polycytidilic acid (poly[I:C]), followed by the transfusion of murine red blood cells (RBCs) expressing the human KEL glycoprotein. Anti-KEL alloimmunization, serum cytokines, and consumption of the transfused RBCs were evaluated longitudina"],"journal":["Blood"],"pubmed_title":["Poly(I:C) causes failure of immunoprophylaxis to red blood cells expressing the KEL glycoprotein in mice."],"pmcid":["PMC7256361"],"funding_grant_id":["P01 HL132819","R01 HL126076","K08 HL141446","T32 HL007974","UL1 TR001863"],"pubmed_authors":["Forsmo JE","Liu J","Luckey CJ","Hendrickson JE","Escamilla-Rivera V","Eisenbarth SC","Gibb DR","Stowell SR","Santhanakrishnan M","Foxman EF","Liu D","Hudson KE","Zimring JC"],"additional_accession":[]},"is_claimable":false,"name":"Poly(I:C) causes failure of immunoprophylaxis to red blood cells expressing the KEL glycoprotein in mice.","description":"Polyclonal anti-D (Rh immune globulin [RhIg]) therapy has mitigated hemolytic disease of the newborn over the past half century, although breakthrough anti-D alloimmunization still occurs in some treated females. We hypothesized that antiviral responses may impact the efficacy of immunoprophylaxis therapy in a type 1 interferon (IFN)-dependent manner and tested this hypothesis in a murine model of KEL alloimmunization. Polyclonal anti-KEL immunoprophylaxis (KELIg) was administered to wild-type or knockout mice in the presence or absence of polyinosinic-polycytidilic acid (poly[I:C]), followed by the transfusion of murine red blood cells (RBCs) expressing the human KEL glycoprotein. Anti-KEL alloimmunization, serum cytokines, and consumption of the transfused RBCs were evaluated longitudina","dates":{"release":"2020-01-01T00:00:00Z","publication":"2020 May","modification":"2025-04-19T18:07:02.803Z","creation":"2022-02-10T11:57:28.686Z"},"accession":"S-EPMC7256361","cross_references":{"pubmed":["32266378"],"doi":["10.1182/blood.2020005018"]}}