Fatemeh Nasri; Mehrnoosh Doroudchi; Bahia Namavar Jahromi; Behrouz Gharesi-Fard
Abstract
Background: Polycystic ovary syndrome (PCOS) is considered as the most common cause of female infertility that affects 4-10% of women in the reproductive age. Previous studies have shown the role of a balanced immune response in a successful pregnancy and fertility. Objective: To investigate the T helper ...
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Background: Polycystic ovary syndrome (PCOS) is considered as the most common cause of female infertility that affects 4-10% of women in the reproductive age. Previous studies have shown the role of a balanced immune response in a successful pregnancy and fertility. Objective: To investigate the T helper cells type 1 (Th1) /Th2/Th17/Treg paradigms in peripheral blood of infertile PCOS compared with normal fertile women. Methods: Peripheral blood mononuclear cells (PBMCs) were isolated at the late follicular phase from 10 PCOS and 10 fertile women. PBMCs were stimulated with PMA and ionomycin in the presence of Berefeldin A as Golgi stop agent to detect intracellular cytokine production (IFN-γ, IL-17, and IL-4) from CD3+CD4+T cells population indicating T helper (Th) cells subsets by flowcytometry. Moreover, regulatory T cells were enumerated using CD25 and Foxp3 markers. Results: In this study, we report that the frequency of Th1 cells was increased compared to Th2 cells in infertile PCOS when considering Th1/Th2 ratio (P=0.05). Analysis of Th17/Th2 ratio showed a significant difference with a bias toward Th17 dominancy in PCOS (P=0.02). The proportion of CD4+CD25+Foxp3+ regulatory T cells was significantly lower in PCOS patients than that of healthy fertile women (P=0.02). Conclusion: In summary, Th1 and Th17 bias and reduction of Treg and Th2 cells as regulators of immune responses might be involved in the pathogenesis of PCOS. These results are suggestive of an altered immune response to inflammatory status in PCOS patients, likely causing some complications such as infertility in these patients.
Behrouz Gharesi-Fard; Fatemeh Mobasher-Nejad; Fatemeh Nasri
Volume 13, Issue 4 , December 2016, , Pages 296-308
Abstract
Background: Pre-eclampsia (PE) is known as a main factor contributing to
fetomaternal mortality, which might affect 2-8% of all pregnancies after the twentieth
week of gestation. The balance of T helper subsets is essential to sustain a normal
pregnancy and preventing fetomaternal complications. Objective: ...
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Background: Pre-eclampsia (PE) is known as a main factor contributing to
fetomaternal mortality, which might affect 2-8% of all pregnancies after the twentieth
week of gestation. The balance of T helper subsets is essential to sustain a normal
pregnancy and preventing fetomaternal complications. Objective: To investigate
differences in the levels of transcription factors and cytokine gene expression of
Th1/Th2/Th17/Treg subsets within decidual and chorionic layers of placentas from 15
PE-afflicted and 15 healthy Iranian women in their third trimester of pregnancy.
Methods: Using Quantitative real-time PCR (Q-PCR), The expression of T-BET,
GATA-3, ROR-ɣt, FOXP3, and cytokines, including IL-1, IL-6, TNF-α, IFN-γ, IL-4,
IL-31, IL-17, IL-23, TGF-β1, TGF-β2, TGF-β3, and IL-35 in the placenta were
compared at mRNA levels between groups. Results: FOXP3 and GATA-3 were
significantly down-regulated, while T-BET was up-regulated in PE deciduae compared
to the control group (p<0.0001, p<0.02, and p<0.01, respectively). Concerning the
chorionic samples, FOXP3 significantly decreased, while ROR-γt increased in the PE
placentas compared to the healthy ones (p<0.0006 and p<0.02, respectively). Besides,
most inflammatory cytokines were up-regulated, while anti-inflammatory cytokines
were down-regulated in the PE placentas. Additionally, TNF-α/IL-35, IFN-ɣ/IL-35, IL-
6/IL-35, and IL-23/IL-35 ratios were significantly higher (p<0.01) and IL-35/IL-17 ratio
was significantly lower (p<0.05) in the pre-eclamptic patients compared to the healthy
controls. Conclusion: Our results shed more light on the contribution of
Th1/Th2/Th17/Treg balance within placenta in the fate of a normal pregnancy.
Moreover, regulatory T cells and IL-35 seem to play a central role in the regulation of
all subsets.
