Prostaglandins in semen compromise the immune response against sexually transmitted pathogens

F. REMES LENICOV; A. VARESE; A. MERLOTTI; J. GEFFNER; A. CEBALLOS

MEDICAL HYPOTHESES

CHURCHILL LIVINGSTONE

Lugar: ESCOCIA; Año: 2014

0306-9877

Seminal plasma is not just a spermatozoa carrier. It induces the expression ofinflammatory cytokines and chemokines and a massive infiltration of neutrophils,monocytes and dendritic cells in the female genital mucosa after coitus, enablingthe innate immune system to fight against sexually transmitted pathogens.However, exposure to seminal plasma not only turns on an inflammatory responsebut also induces regulatory mechanisms that allow the fetus (a semiallograft) togrow and develop in the uterus. In mouse models it has been shown that seminalplasma induces the expansion of regulatory T cells specific to seminal Ags in thereceptive partner, thus promoting tolerance to paternal alloantigens and avoidingallogeneic fetal rejection. These mechanisms appear to be mainly induced byprostaglandins of the E series (PGE) and TGF-beta, which are present at hugeconcentrations in the seminal plasma. Moreover, we have recently shown thatexposure to seminal plasma induces the differentiation of dendritic cells into atolerogenic profile through a mechanism dependent on the activation of theprostanoid receptors EP2 and EP4 by seminal PGE.Our hypothesis proposes that this tolerogenic response induced by seminal PGE,while promoting fertility by inducing tolerance toward paternal alloantigens, mightalso compromise the development of the adaptive immune response againstsexually transmitted pathogens in the receptive partner.