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Intra‐Amniotic Administration of HMGB1 Induces Spontaneous Preterm Labor and Birth
Authors:Nardhy Gomez‐Lopez  Roberto Romero  Olesya Plazyo  Bogdan Panaitescu  Amy E. Furcron  Derek Miller  Tamara Roumayah  Emily Flom  Sonia S. Hassan
Affiliation:1. Perinatology Research Branch, Program for Perinatal Research and Obstetrics, Division of Intramural Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, NICHD/NIH/DHHS, Bethesda, MD, and Detroit, MI, USA;2. Department of Obstetrics and Gynecology, Wayne State University School of Medicine, Detroit, MI, USA;3. Department of Immunology and Microbiology, Wayne State University School of Medicine, Detroit, MI, USA;4. Department of Obstetrics and Gynecology, University of Michigan, Ann Arbor, MI, USA;5. Department of Epidemiology and Biostatistics, Michigan State University, East Lansing, MI, USA;6. Center for Molecular Medicine and Genetics, Wayne State University, Detroit, MI, USA;7. Department of Pediatrics, Neonatology Division, Wayne State University School of Medicine, Detroit, MI, USA
Abstract:Nearly 65 years have passed since Peter Medawar posed the following question: “How does the pregnant mother contrive to nourish within itself, for many weeks or months, a fetus that is an antigenically foreign body.” Now, understanding of reproductive immunology has demonstrated that the HLA antigens in the placenta are non‐classical and do not induce rejection. In the placenta and in tumors, 50% or more of the cells are cells of the immune system and were once thought to be primed and ready for killing tumors or the “fetal transplant” but these cells are not potential killers but abet the growth of either the tumor or the placenta. We believe that these cells are there to create an environment, which enhances either placental or tumor growth. By examining the similarities of the placenta's and tumor's immune cells, novel mechanisms to cause tumors to be eliminated can be devised.
Keywords:Alarmins  DAMPs  danger signals  parturition  prematurity  sterile intra‐amniotic inflammation
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