4 research outputs found
Reproductive corticotropin releasing hormone, implantation, and fetal immunotolerance
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