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Aim: The objective of this review is to describe the immunological mechanisms which facilitate maternal tolerance at the maternal‐placental interface, and to discuss how these mechanisms are disrupted in pre‐eclampsia. Methods: A literature review was performed based on the analysis of papers available on PubMed. The most important and relevant studies regarding the immunological mechanisms which facilitate maternal tolerance in healthy pregnancy and pre‐eclampsia are presented in this article. Results: The maternal‐placental interface is the site where the immune tolerance begins and develops. Within the innate immunity, natural killer cells, macrophages and dendritic cells play a pivotal role in tolerance through regulation of inflammation. On the other hand, within the adaptive immunity, the correct increase of regulatory T cells is crucial for ensuring immune tolerance toward placental cells. Disturbances in maternal tolerance can lead to the appearance of pregnancy complications such as pre‐eclampsia, which has a considerable impact on perinatal morbidity and mortality. Conclusion: Our partial knowledge of immunological mechanisms involved in tolerance at the maternal‐placental interface indicates that pre‐eclampsia is characterized by alterations of this maternal immune tolerance, which could represent the origin of the disease. [ABSTRACT FROM AUTHOR]

Recurrent pregnancy loss (RPL) is one of the most common obstetrical complications. Multiple etiologies, such as endocrine, anatomic, genetic, hematological and immunological causes have been reported for this devastating disease. However, over half of the cases remain unexplained. Thrombotic/inflammatory processes are often observed at the maternal-fetal interface as the final pathological assault in many cases of RPL, including those of unexplained etiologies. In the present paper, cellular immune responses (T, natural killer [NK], natural killer-T [NKT], regulatory T [Treg] cells and their cytokines) and autoimmune abnormalities of women with RPL are reviewed. In addition, metabolic diseases and hematological conditions which often lead to thrombotic/inflammatory conditions are discussed in association with RPL. Finally, current therapeutic options for RPL are reviewed. [ABSTRACT FROM AUTHOR]

Aim: V‐set and immunoglobulin domain‐containing 4 (VSIG4) is a potent negative regulator of T‐cell responses and is suggested to regulate antitumor immunity. This study investigates whether VSIG4 is significantly expressed in endometriosis patients and the association between VSIG4 levels and serum cancer antigen (CA)‐125 levels, VSIG4 levels and endometriosis severity. Methods: Tumor tissues and peripheral blood samples were obtained during surgery from 42 endometriotic cyst and 21 nonendometriotic tumor patients. The levels of VSIG4 mRNA, VSIG4 protein expression in tumor tissue and serum soluble VSIG4 concentration were compared between the two groups. After dividing the cohort using the optimized cut‐off values obtained by receiver operating characteristic curve analysis, we examined the association between VSIG4 levels and serum CA‐125 levels, VSIG4 levels and the factors indicating endometriosis severity. Results: The expressions of VSIG4 mRNA, VSIG4 protein and serum VSIG4 concentration were significantly increased in the endometriotic cyst group compared with the control group (P = 0.001, 0.002 and 0.049, respectively). The optimized VSIG4 cut‐off values for endometriosis prediction were 0.71, 0.32 and 144.37 pg/mL, respectively. After cohort division using these values, high VSIG4 levels group showed significantly elevated CA‐125 compared with low VSIG4 level group (P = 0.010, 0.043 and 0.039, respectively). There was no association between VSIG4 levels and the factors indicating endometriosis severity. Conclusion: The expression of VSIG4 in endometriosis patients is increased compared with nonendometriotic tumor patients, and higher VSIG4 levels are significantly associated with higher serum CA‐125 levels. VSIG4 may be importantly involved in the immunological alteration of endometriosis. [ABSTRACT FROM AUTHOR]

Aim In normal pregnancy, the Th1 subtype, responsible for the production of inflammatory cytokines, is reduced, and the Th2 subtype is increased to prohibit inflammation. In pre-eclampsia, the Th1 cell population is increased; thus, subsequent inflammation and trophoblast destruction occur. Polymorphisms in the Fas and Fas Ligand ( FasL) promoter regions can influence Fas and FasL expression and accused to increase of Th1 subtype. Methods DNA samples from 153 pregnant women with pre-eclampsia and 140 controls were genotyped through polymerase chain reaction-restriction fragment length polymorphism. A Fisher's exact test was used to compare the distribution of individual polymorphisms. Results Fas-1377 AA, AG and GG genotypes were observed in 2.61%, 18.30% and 79.08% in the pre-eclampsia group opposed to 0%, 27.14% and 72.85% in the control group ( P = 0.037), respectively. Fas-670 AA, AG and GG genotypes were observed in 37.9%, 41.8% and 20.3% of pre-eclampsia patients compared with 33.6%, 50.7% and 15.7% in healthy pregnant women ( P = 0.291), respectively. No statically significant differences in the FasL-844 genotype were observed between the groups ( P = 0.69). Conclusion The Fas-1377G > A polymorphism is associated with a higher risk of pre-eclampsia. [ABSTRACT FROM AUTHOR]

Aim Successful pregnancy requires balanced regulation of immune cells at the feto-maternal interface. Systemic monitoring of the immune system cannot precisely outline local immune status in the uterus. In this survey, endometrial immune milieu was investigated using a non-invasive method of analysis of menstrual blood (MB). The results were compared with peripheral blood (PB). Method PB and MB of healthy fertile women ( n = 15) were collected simultaneously on the second day of their menstrual cycle. T and natural killer T cell subpopulations were immunophenotyped by flow cytometry. Results Among examined cell populations, the frequency of CD4 + Foxp3+, CD4 + Foxp3 + CD25-, CD4 + Foxp3 + CD25+ and IL17+ T cells ( P = 0.022, 0.028, 0.017 and 0.005, respectively) and TCRαβ+, CD45RO+, CD16-, IFNγ + and IL17+ NKT (CD56 + CD3+) cells ( P = 0.010, 0.037, 0.038, 0.015 and 0.021, respectively) were significantly higher in MB compared with PB. Conversely, PB contained a higher percentage of CD16+ T cells ( P = 0.025) in comparison with MB. Conclusion MB contains cells of an inflammatory and anti-inflammatory nature, implying the existence of finely tuned cell homeostasis during menstruation. Our results imply that MB could be viewed as an easy-to access specimen for monitoring endometrial immune cells, especially those that have preferential endometrial localization. [ABSTRACT FROM AUTHOR]