<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Escamilla-Rivera V</submitter><funding>NCATS NIH HHS</funding><funding>NHLBI NIH HHS</funding><pagination>1983-1993</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7256361</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>135(22)</volume><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</pubmed_abstract><journal>Blood</journal><pubmed_title>Poly(I:C) causes failure of immunoprophylaxis to red blood cells expressing the KEL glycoprotein in mice.</pubmed_title><pmcid>PMC7256361</pmcid><funding_grant_id>P01 HL132819</funding_grant_id><funding_grant_id>R01 HL126076</funding_grant_id><funding_grant_id>K08 HL141446</funding_grant_id><funding_grant_id>T32 HL007974</funding_grant_id><funding_grant_id>UL1 TR001863</funding_grant_id><pubmed_authors>Forsmo JE</pubmed_authors><pubmed_authors>Liu J</pubmed_authors><pubmed_authors>Luckey CJ</pubmed_authors><pubmed_authors>Hendrickson JE</pubmed_authors><pubmed_authors>Escamilla-Rivera V</pubmed_authors><pubmed_authors>Eisenbarth SC</pubmed_authors><pubmed_authors>Gibb DR</pubmed_authors><pubmed_authors>Stowell SR</pubmed_authors><pubmed_authors>Santhanakrishnan M</pubmed_authors><pubmed_authors>Foxman EF</pubmed_authors><pubmed_authors>Liu D</pubmed_authors><pubmed_authors>Hudson KE</pubmed_authors><pubmed_authors>Zimring JC</pubmed_authors></additional><is_claimable>false</is_claimable><name>Poly(I:C) causes failure of immunoprophylaxis to red blood cells expressing the KEL glycoprotein in mice.</name><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</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 May</publication><modification>2025-04-19T18:07:02.803Z</modification><creation>2022-02-10T11:57:28.686Z</creation></dates><accession>S-EPMC7256361</accession><cross_references><pubmed>32266378</pubmed><doi>10.1182/blood.2020005018</doi></cross_references></HashMap>