And University Hospitals, Case Medical Center for giving GBM surgical specimens
And University Hospitals, Case Medical Center for providing GBM surgical specimens for thisstudy. We are grateful to members in Dr. RANTES/CCL5, Human Rich’s laboratory for scientific discussion. We also thank Cathy Shemo and Sage O’Bryant of the Flow Cytometry Core and J udith Drazba in the Imaging Core and Central Cell Services at Cleveland Clinic Lerner Analysis Institute for their help. This work was supported by National Hepcidin/HAMP Protein Biological Activity Institutes of Health R01 grants (CA184090, NS091080, and NS099175) to S. Bao as well as a National Institutes of Health Shared Instrument Grant (S10OD018205) to the Cleveland Clinic Lerner Study Institute. The authors declare no competing monetary interests.Submitted: 23 October 2015 Revised: 20 July 2016 Accepted: 8 November
HHS Public AccessAuthor manuscriptJ Immunol. Author manuscript; accessible in PMC 2018 February 01.Published in final edited kind as: J Immunol. 2017 August 01; 199(three): 1041050. doi:10.4049/jimmunol.1700401.Author Manuscript Author Manuscript Author Manuscript Author ManuscriptType I IFN Is Needed and Enough 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,Department Division Department �Bloodworks epartmentof Laboratory Medicine, Yale University College of Medicine, New Haven, CT 06520 of Pediatrics, Yale University School of Medicine, New Haven, CT 06520 of Immunobiology, Yale University School of Medicine, New Haven, CT 06520 Northwest Research Institute, Seattle, WA 98102 of Laboratory Medicine, University of Washington School of Medicine, Seattle, WADivisionof Hematology, Department of Medicine, University of Washington School of Medicine, Seattle, WA#HowardHughes Medical Institute, Chevy Chase, MDAbstractDuring RBC transfusion, production of alloantibodies against RBC non-ABO Ags may cause hemolytic transfusion reactions and limit availability of compatible blood items, resulting in anemia-associated morbidity and mortality. A number of research have established that specific inflammatory issues and inflammatory stimuli promote alloimmune responses to RBC Ags. Nevertheless, the molecular mechanisms underlying these findings are poorly understood. Variety I IFNs (IFN-/) are induced in inflammatory situations linked with elevated alloimmunization. By establishing a brand new transgenic murine model, we demonstrate that signaling by way of the IFN-/ receptor is necessary for inflammation-induced alloimmunization. Moreover, mitochondrial antiviral signaling protein–mediated signaling by way of cytosolic pattern recognition receptors was required for polyinosinic-polycytidylic acid–induced IFN-/ production and alloimmunization. We additional report that IFN-, within the absence of an adjuvant, is adequate toAddress correspondence and reprint requests to Dr. Jeanne E. Hendrickson, Yale University Departments of Laboratory Medicine and Pediatrics, 330 Cedar Street, Clinic Developing 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 from the manuscript, and all authors ed.
