Listeria monocytogenes Cytoplasmic Entry Induces Fetal Wastage by Disrupting Maternal Foxp3+ Regulatory T Cell-Sustained Fetal Tolerance
Figure 8
Proposed model for immune-mediated fetal wastage induced by prenatal infection that can occur with or without in utero pathogen invasion.
After low dose infection during pregnancy, reductions in maternal regulatory T cell suppression unleash the activation of immune effectors enough to rapidly eliminate the pathogen. However, given the requirement for sustained expansion of maternal regulatory cell suppression in maintaining fetal tolerance, these reductions in suppressive potency also trigger immune-mediated fetal wastage. By comparison with higher dosage infection, blunted maternal regulatory T cell suppression that promotes immune activation does not eradicate infection as efficiently. In turn with ongoing disruption in fetal tolerance, remaining pathogen is drawn to inflammation at the uterine-placental interface that promotes invasion into the placental-fetal unit.
doi: https://doi.org/10.1371/journal.ppat.1002873.g008