Regulatory T‐cell Subpopulations in Severe or Early‐onset Preeclampsia

Abstract

ProblemA deficiency in regulatory T (Treg) cells causing reduced immune regulatory capacity has been proposed in preeclampsia. ObjectiveUtilizing recent advances in flow cytometry phenotyping, we aimed to assess whether a deficiency of Treg subpopulations occurs in preeclampsia. Method of StudySix-color flow cytometry was used for Treg phenotyping in 18 preeclamptic women (1 early-onset, 1 severe and 16 both), 20 women with normal pregnancy and 20 non-pregnant controls.

Enhanced Th1 and inflammatory mRNA responses upregulate NK cell cytotoxicity and NKG2D ligand expression in human pre‐eclamptic placenta and target it for NK cell attack

“…Our results are supported by an investigation of T regulatory cell subpopulations in severe or early onset PE that showed no differences in Treg numbers but in their CTLA4 and CCR4 expression, suggesting a migratory defect 29. Taken together, the disparate regulatory cytokine responses that we found might indicate a dysregulation in the pool of Treg cells in PE.…”

Aspects of inflammation, angiogenesis and coagulation in preeclampsia

“…When analysed separately, both placentas from women with EOP and LOP expressed significantly less CCL18 than those from women with normal pregnancies (Figure 25a). The finding is in line with the reported decreased presence of Tregs at the foetomaternal interface in preeclampsia (66,67), which is also in accordance with our previous finding of a possible migratory defect of circulating Treg cells based on the phenotype in paper III (218). Furthermore, the lack of CCL18 might also skew local immunity from Th2/Treg towards Th1/Th17 in preeclampsia (14,219,220).…”

Immunomodulatory effects of probiotic supplementation during pregnancy and infancy in allergy prevention studies

“…Although a bias toward Th2 and Treg immunity has been associated with healthy pregnancy [177], the relationship between different circulating Th cell subsets is not straightforward. Instead, these adaptations appear most evidently at the fetal-maternal interface, where for instance Tregs are enriched and promote fetal tolerance [178,179]. Also innate immune cells, that is, natural killer cells and macrophages, are enriched, constituting the majority of decidual leukocytes [177].…”

“…However, earlier research has indicated that activated Tregs may have an increased migratory capacity, as shown by their chemokine receptor expression [179]. Almost all aTregs express the chemokine receptor CCR4 in contrast to the resting Tregs (CD45RA + Foxp3 + ) [179].…”

“…Almost all aTregs express the chemokine receptor CCR4 in contrast to the resting Tregs (CD45RA + Foxp3 + ) [179].…”