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Isolation of Leukocytes from the Murine Tissues at the Maternal-Fetal Interface
Published on: May 21, 2015
Altered expression of TCR-CD3zeta induced by sera from women with preeclampsia
P W Whitecar1, K A Boggess, M J McMahon
1Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, University of North Carolina at Chapel Hill School of Medicine, NC 27599-7516, USA
Objective:
To investigate TCR-CD3zeta expression by cultured T lymphocytes exposed to midtrimester sera from pregnant women in whom preeclampsia developed at term compared with normotensive pregnant control subjects.
Study Design:
Sera obtained at 24 to 28 weeks' gestation from 16 nulliparous women in whom preeclampsia developed at term and from 32 gestational age-matched control subjects without preeclampsia were evaluated for TCR-CD3zeta chain expression with use of Jurkat cells. Subsets of serum samples from 6 women with preeclampsia and 6 control subjects were then evaluated for their ability to induce apoptosis and to suppress interleukin-2 production. Groups were compared by use of the Kruskal-Wallis test, and P <.05 was considered significant.
Results:
TCR-CD3zeta chain expression in cultured T lymphocytes was suppressed in approximately 60% of untreated control subjects after incubation with sera from normotensive pregnant women compared with 30% after incubation with sera from women with preeclampsia (P <.001). T-cell apoptosis was significantly higher after incubation with sera from normotensive control subjects, as was the expression of the proapoptotic regulator Bax, compared with sera from women with preeclampsia. Interleukin-2 levels were higher in T cells incubated with sera from women in whom preeclampsia later developed compared with sera from normotensive pregnant women (27.7 ng/mL versus 72.5 ng/mL; P <.001).
Conclusions:
Nulliparous women in whom preeclampsia developed did not suppress TCR-CD3zeta levels to the extent of normotensive control subjects, which may be linked to decreased lymphocyte apoptosis. This occurs remotely from the manifestation of clinical disease and suggests a deficiency in a serum factor in preeclampsia that may induce T cell zeta chain suppression in normal pregnancy.

