[163-POS] : Altered T cell populations in the fetal thymus and spleen in pre-eclampsia: A cohort study

Pregnancy hypertension(2015)

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摘要
Pre-eclampsia is incompletely understood, however, maternal immune rejection of the fetus is a well-supported theory. In particular, maternal T cell studies have shown a reduction in regulatory T cells in pre-eclampsia, and a shift towards a pro-inflammatory state. Morphologic change of the fetal thymus, a primary center for T cell differentiation, has also been described, even preceding clinical disease. This might indicate a fetal role in disease pathogenesis, although histologic examination of T cell subsets in pre-eclamptic fetuses has not been performed. The aim of this study was to investigate thymic and splenic T cell subsets in pre-eclamptic fetuses. We hypothesized that pre-eclampsia would be linked to altered T cell populations, in both thymus and spleen.This was a cohort study, with tissue collected from deceased fetuses at The Children's Hospital at Westmead (Sydney Australia), and Canberra Hospital (Canberra, Australia). Six fetuses born to pre-eclampsia were included, with 7 fetuses in the control group. Immunohistochemistry techniques analysed FoxP3+, CD4+ and CD8+ T cell subsets, in fetal thymus and spleen. Each T cell subset was compared between groups using an exact interpretation of the Cochrane Armitage test for trend.FoxP3+ regulatory T cells were significantly reduced in the thymus (p=0.02) and spleen (p=0.02) of fetuses born to pre-eclampsia, versus controls. In both thymus and spleen, CD8+ T cells were also decreased in pre-eclamptic fetuses, versus controls (p=0.04 and p=0.004, respectively). Conversely, CD4+ T cells were comparable between groups in both thymus and spleen.Pre-eclampsia is associated with an altered T cell profile in the fetal thymus and spleen. Altered fetal immune function might contribute to disease pathogenesis.D.P. Eviston: None. M. Peek: None. P. Hsu: None. B. Santner-Nanan: None. M. Hu: None. J. Dahlstrom: None. S. Arbuckle: None. R. Nanan: None.
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