Abstract
The risk factors for preeclampsia, extremes of maternal age, changing paternity, concomitant maternal autoimmunity, and/or birth intervals greater than 5 years, suggest an underlying immunopathology. We used peripheral blood and lymphocytes from the UteroPlacental Interface (UPI) of 3rd trimester healthy pregnant women in multicolor flow cytometry—and in vitro suppression assays. The major end-point was the characterization of activation markers, and potential effector functions of different CD4—and CD8 subsets as well as T regulatory cells (Treg). We observed a significant shift of peripheral CD4 –and CD8- T cells from naïve to memory phenotype in preeclamptic women compared to healthy pregnant women consistent with long-standing immune activation. While the proportions of the highly suppressive Cytokine and Activated Treg were increased in preeclampsia, Treg tolerance toward fetal antigens was dysfunctional. Thus, our observations indicate a long-standing inflammatory derangement driving immune activation in preeclampsia; in how far the Treg dysfunction is caused by/causes this immune activation in preeclampsia will be the object of future studies.
Highlights
Preeclampsia is a mysterious condition that affects 3–17% of pregnancies worldwide[1]
To address whether the T cell subsets of preeclamptic patients displayed differential distribution or Rejection in preeclampsia activation compared with healthy patients, we utilized the same sampling- and gating strategy as published previously [7], including samples obtained from the uteroplacental interface (UPI), the uterus locale where the placenta attaches to the uterus and the maternal—and fetal systems meet
The risk factors for preeclampsia have suggested that an underlying immunopathology is part of the origins of this mysterious, but common disease [13]
Summary
Preeclampsia is a mysterious condition that affects 3–17% of pregnancies worldwide[1]. The reader’s life in some way has been touched by preecampsia. The mother and fetus may suffer serious complications including hypertension, organ failure, progression to seizures (eclampsia), prematurity, and death[1]. A molecular explanation for preeclampsia that could guide more robust treatments is a major unmet medical need. Risk factors for preeclampsia include extremes of maternal age, changing paternity, concomitant maternal autoimmunity, and/or birth intervals greater than 5 years all suggesting involvement of immunologic mechanisms[1]. The pathology of preeclampsia has been investigated at many levels including placentation abnormalities and novel molecular descriptions of the hypertensive phenotype [2,3,4].
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