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Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats
Published on: November 20, 2015
Mouse Model of Hemolytic Disease of the Fetus and Newborn
Hirotomo Nakahara1,2, Sasikala Muthusamy3, Rebecca C Hale3
1Division of Transfusion Medicine, Mass General Brigham, Harvard Medical School, Boston, MA, USA. hnakahara@bwh.harvard.edu.
Abstract:
Hemolytic Disease of the Fetus and Newborn (HDFN) is caused by the placental transfer of maternal red blood cell (RBC) alloantibodies into the fetal circulation which then targets paternally derived RBC antigens expressed on the fetal RBC. The resulting anemia in the fetus/newborn can lead to grave clinical consequences including hydrops fetalis, kernicterus, and perinatal demise. We have utilized the human KEL transgenic mouse model to study the induction of anti-KEL RBC alloantibodies through pregnancy as well as transfusion and the subsequent placental transfer of anti-KEL RBC alloantibodies into the fetal circulation, causing anemia, hydrops, and fetal/neonatal demise. Here, we describe the methods used to establish the KEL transgenic mouse HDFN model and the assays that evaluate the key pathologic features of HDFN.

