Corticotropin-releasing hormone (CRH) and immunotolerance of the fetus.
The hypothalamic neuropeptide corticotropin-releasing hormone (CRH) is produced by several tissues of the female reproductive system, including the endometrial glands and decidualized stroma, as well as the trophoblast, syncytiotrophoblast, and placental decidua. CRH is also secreted at inflammatory sites and possesses potent pro-inflammatory properties influencing both innate and acquired immune processes. Recent experimental findings show that uterine CRH participates in local immune phenomena associated with early pregnancy, such as differentiation of endometrial stroma to decidua and protection of the fetus from the maternal immune system. CRH induces the expression of apoptotic Fas ligand (FasL) on invasive extravillous trophoblast and maternal decidual cells at the fetal-maternal interface. Furthermore, CRH increases the apoptosis of activated T lymphocytes through FasL induction, participating in the processes of both implantation and early pregnancy tolerance.
Makrigiannakis
Antonis
A
Laboratory of Pharmacology, School of Medicine, University of Crete, Heraklion 71110, Greece. makrigia@med.uoc.gr
Zoumakis
Emmanuel
E
Kalantaridou
Sofia
S
Mitsiades
Nikos
N
Margioris
Andreas
A
Chrousos
George P
GP
Gravanis
Achilleas
A
D000818:Animals; D017209:Apoptosis; D002454:Cell Differentiation; D003346:Corticotropin-Releasing Hormone / Q000276:immunology* / Q000378:metabolism; D003656:Decidua / Q000166:cytology; D010064:Embryo Implantation; D004717:Endometrium / Q000378:metabolism; D005260:Female; D005333:Fetus / Q000166:cytology / Q000276:immunology*; D006801:Humans; D007108:Immune Tolerance
D003346:Corticotropin-Releasing Hormone