For a long time, the conventional view was that the fetus and maternal vascular system are kept separate. In fact there is a two way traffic of cells through the placenta and the transplacental passage of cells is in fact the norm. The fetal cells can persist in a wide range of woman's tissues following a pregnancy or an abortion and she becomes a chimera. Fetal cells have been found in the maternal circulation and they were shown to persist for the entire life in humans, thus demonstrating long-term engraftment and survival capabilities. Microchimerism is a subject of much interest for a number of reasons. Studies of fetal microchimerism during pregnancy may offer explanations for complications of pregnancy, such as preeclampsia, as well as insights into the pathogenesis of autoimmune diseases which usually ameliorate during pregnancy. The impact of the persistence of allogenic cells of fetal origin and of the maternal immunological response to them on the mother's health is still not clear. On the beneficial side, it has been proposed that genetically disparate fetal microchimerism provides protection against some cancers, that fetal microchimerism can afford the mother new mechanisms of protection to some diseases, that fetal microchimerism can enlarge the immunological repertoire of the mother improving her defense against aggressor. Fetal cells are often present at sites of maternal injury and may have an active role in the repair of maternal tissues.
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http://dx.doi.org/10.1016/j.ejogrb.2011.05.008 | DOI Listing |
Forensic Sci Int
December 2024
Department of Science, Institute of Forensic Sciences and Legal Medicine, Istanbul University-Cerrahpaşa, Istanbul, Turkey. Electronic address:
Microchimerism (MC) refers to the presence of small amounts of foreign cells or DNA in the tissues or circulation of an individual. It generally occurs through mother-fetus interaction, twin pregnancies, and intergenerational transmission. MC is influenced by genetic and environmental factors such as toxic conditions, immunological suppression, and various diseases (influenza, COVID-19, etc.
View Article and Find Full Text PDFAnn Hematol
December 2024
Division of Hematology, Department of Medicine, Keio University School of Medicine, Tokyo, Japan.
Transient abnormal myelopoiesis (TAM) generally affects newborns with Down syndrome and is associated with constitutional trisomy 21 and a somatic GATA1 mutation. Here we describe a case of TAM which evolved after umbilical cord blood transplantation (UCBT), whose origin was identified as a GATA1 mutation-harboring clone in umbilical cord blood (UCB) by detailed genetic analyses. A 58-year-old male who received UCBT for peripheral T-cell lymphoma presented progressive anemia and thrombocytopenia, and leukocytosis with blast cells in the peripheral blood (PB).
View Article and Find Full Text PDFSemin Immunopathol
December 2024
Division of Pediatric Stem Cell Transplantation and Immunology, Clinic of Pediatric Hematology and Oncology, University Medical Center Hamburg-Eppendorf, 20246, Hamburg, Germany.
Toleration of a semi-allogeneic fetus in the mother's uterus as well as tolerance after allogeneic hematopoietic stem cell transplantation (HSCT) appear to share some immunologic concepts. The existence of microchimeric cells, and the original idea of a bidirectional cell trafficking between mother and child during pregnancy have been known for decades. Today, origins and mechanisms of persistence of microchimeric cells are intensively being elucidated.
View Article and Find Full Text PDFCommun Biol
December 2024
Washington University in St. Louis School of Medicine, Department of Surgery, Division of Pediatric Surgery, St. Louis, MO, USA.
Medicina (Kaunas)
October 2024
Laboratory of Human Genomics, University of Medicine and Pharmacy of Craiova, 200638 Craiova, Romania.
Recurrent pregnancy loss (RPL) is a multifactorial condition, encompassing genetic, anatomical, immunological, endocrine, as well as infectious and environmental factors; however, the etiology remains elusive in a substantial number of cases. Genetic factors linked to RPL include parental karyotype abnormalities (e.g.
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