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. Author manuscript; available in PMC: 2013 Nov 21.
Published in final edited form as: Reproduction. 2013 Oct 21;146(6):R191–R203. doi: 10.1530/REP-13-0262

Figure 2.

Figure 2

Proposed model for how pregnancy complications may occur with or without direct pathogen invasion of the placental-fetal unit. Infection induced reductions in maternal Treg suppression that unleash the activation of protective immune components fracture fetal tolerance unmasking normally tolerized fetal antigen. In turn, inflammation occurs at the maternal fetal interface containing the highest concentration of exposed fetal cells. With low dosage infection (a), circulating pathogen is eradicated, but pregnancy complications ensue from damage caused by activated maternal immune effector cells. With higher dosage infection (b), the persistence of circulating pathogen and inflammation at the maternal-fetal interface provides a conduit for invasion overriding the normally protective placental barrier.