And University Hospitals, Case Medical Center for delivering GBM surgical specimens for thisstudy. We’re grateful to members in Dr. Rich’s laboratory for scientific discussion. We also thank Cathy Shemo and Sage O’Bryant of the Flow Cytometry Core and J udith Drazba of your Imaging Core and Central Cell Services at Cleveland Clinic Lerner Study Institute for their help. This function was supported by National Institutes of Well being R01 grants (CA184090, NS091080, and NS099175) to S. Bao as well as a National Institutes of Overall health Shared Instrument Grant (S10OD018205) to the Cleveland Clinic Lerner Analysis Institute. The authors declare no competing economic interests.Submitted: 23 October 2015 Revised: 20 July 2016 Accepted: eight November
HHS Public AccessAuthor manuscriptJ Immunol. Author manuscript; obtainable in PMC 2018 February 01.Published in final edited kind as: J Immunol. 2017 August 01; 199(3): 1041050. doi:10.4049/jimmunol.1700401.Author Manuscript Author Manuscript Author Manuscript Author ManuscriptType I IFN Is Necessary and Sufficient for Inflammation-Induced Red Blood Cell Alloimmunization in MiceDavid R. Gibb, Jingchun Liu, Prabitha Natarajan, Manjula Santhanakrishnan, David J. Madrid, Stephanie C. Eisenbarth,, James C. Zimring, Akiko Iwasaki,#, and Jeanne E. Hendrickson,Division Division Division �Bloodworks epartmentof Laboratory Medicine, Yale University School of Medicine, New Haven, CT 06520 of Pediatrics, Yale University College of Medicine, New Haven, CT 06520 of Immunobiology, Yale University College of Medicine, New Haven, CT 06520 Northwest Study Institute, Seattle, WA 98102 of Laboratory Medicine, University of Washington School of Medicine, Seattle, WADivisionof Hematology, Division of Medicine, University of Washington School of Medicine, Seattle, WA#HowardHughes Healthcare Institute, Chevy Chase, MDAbstractDuring RBC transfusion, production of alloantibodies against RBC non-ABO Ags can cause hemolytic transfusion reactions and limit availability of compatible blood goods, resulting in anemia-associated morbidity and mortality. Various studies have established that certain inflammatory disorders and inflammatory stimuli market alloimmune responses to RBC Ags. Nonetheless, the molecular mechanisms underlying these findings are poorly understood. Type I IFNs (IFN-/) are induced in inflammatory circumstances associated with increased alloimmunization. By building a brand new transgenic murine model, we demonstrate that signaling by means of the IFN-/ receptor is essential for inflammation-induced alloimmunization. Also, mitochondrial antiviral signaling protein–mediated signaling by way of cytosolic pattern recognition receptors was necessary for polyinosinic-polycytidylic acid–induced IFN-/ production and alloimmunization.Semaphorin-7A/SEMA7A Protein medchemexpress We additional report that IFN-, within the absence of an adjuvant, is enough toAddress correspondence and reprint requests to Dr.CDCP1 Protein web Jeanne E.PMID:24513027 Hendrickson, Yale University Departments of Laboratory Medicine and Pediatrics, 330 Cedar Street, Clinic Creating 405, PO Box 208035, New Haven, CT 06520. [email protected]. ORCIDs: 0000-0003-3703-7635 (M.S.); 0000-0002-1244-208X (S.C.E.); 0000-0002-7824-9856 (A.I.); 0000-0002-7928-3132 (J.E.H.). D.R.G., A.I., J.C.Z., S.C.E., and J.E.H. planned the experiments completed by D.R.G., J.L., P.N., M.S., D.J.M., and J.E.H; J.C.Z. generated K1 mice. All authors produced experimental ideas. D.R.G. wrote the initial draft with the manuscript, and all authors ed.
