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Isolation of Leukocytes from the Murine Tissues at the Maternal-Fetal Interface
07:51

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Published on: May 21, 2015

Reproductive corticotropin releasing hormone, implantation, and fetal immunotolerance

Sophia N Kalantaridou1, Emmanouil Zoumakis, Stacie Weil

  • 1Division of Reproductive Endocrinology, Department of Obstetrics and Gynecology, University of Ioannina Medical School, Ioannina, Greece. Sophia_Kalantaridou@hotmail.com

Critical Reviews in Clinical Laboratory Sciences
|October 19, 2007
PubMed

The fundamental process of implantation involves a series of steps leading to effective cross-talk between invasive trophoblast cells and the maternal endometrium. The molecular interactions at the embryo-maternal interface during the time of blastocyst adhesion and subsequent invasion are not fully understood. Embryonic trophoblast and maternal decidual cells produce corticotropin-releasing hormone (CRH) and express Fas ligand (FasL), a proapoptotic cytokine. Fas and its ligand are pivotal in the regulation of immune tolerance. Trophoblast and decidual CRH play crucial roles in implantation, as well as in the anti-rejection process that protects the fetus from the maternal immune system, primarily by killing activated T cells through Fas-FasL interaction. The potential use of CRH antagonists is presently under intense investigation. CRH antagonists have been used experimentally to elucidate the role of CRH in blastocyst implantation and invasion, early fetal immunotolerance, and premature labor.

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