Maternal immune dysregulation seems to affect fetal or postnatal immune development. Preeclampsia is a pregnancy-associated disorder with an immune basis and is linked to atopic disorders in offspring. Here we show reduction of fetal thymic size, altered thymic architecture and reduced fetal thymic regulatory T (Treg) cell output in preeclamptic pregnancies, which persists up to 4 years of age in human offspring. In germ-free mice, fetal thymic CD4 + T cell and Treg cell development are compromised, but rescued by maternal supplementation with the intestinal bacterial metabolite short chain fatty acid (SCFA) acetate, which induces upregulation of the autoimmune regulator (AIRE), known to contribute to Treg cell generation. In our human cohorts, low maternal serum acetate is associated with subsequent preeclampsia, and correlates with serum acetate in the fetus. These findings suggest a potential role of acetate in the pathogenesis of preeclampsia and immune development in offspring.

Our data indicate that in addition to Foxp3(+) Treg cells, CD4(+) T cells acquire HLA-G from decidual DCs and may play an important role in immune tolerance induction in pregnancy, a process which is impaired in pre-eclampsia.

In the absence of significant risk factors for haemorrhage at CS in a tertiary setting, routine blood type and screen testing does not enhance patient care. In the rare event that a patient without previously identifiable risk factors requires an urgent blood transfusion, O negative blood could be given in the interim pending formal determination of type and cross-match.

The human T cell compartment is a complex system and while some information is known on repertoire composition and dynamics in the peripheral blood, little is known about repertoire composition at different anatomical sites. Here, we determine the T cell receptor beta variable (TRBV) repertoire at the decidua and compare it with the peripheral blood during normal pregnancy and pre-eclampsia. We found total T cell subset disparity of up to 58% between sites, including large signature TRBV expansions unique to the fetal–maternal interface. Defining the functional nature and specificity of compartment-specific T cells will be necessary if we are to understand localized immunity, tolerance, and pathogenesis.

Cytomegalovirus is the most common congenital viral infection. Infection can cause developmental delay, sensorineural deafness and fetal death. Fetal damage is more severe when infection occurs in the first trimester of pregnancy. Prenatal ultrasound findings may be cerebral, such as ventriculomegaly, microcephaly and periventricular leukomalacia, as well as non-cerebral, such as echogenic bowel, ascites and pericardial effusion. We present a case of congenital cytomegalovirus infection in which the only ultrasound sign noted at routine second-trimester scan was low-grade echogenic bowel, a soft marker, which progressed to severe disease in the third trimester, when further investigation was prompted, leading to the diagnosis. Patients need to be counselled regarding the possible perinatal prognosis. Ultrasound markers can often but not always predict severity and, hence, counselling can be a challenge. Conclusion: A meticulous anatomy survey in mid-trimester remains the norm and ultrasound soft markers should prompt comprehensive testing for viral infections in pregnancy.