transforming-growth-factor-beta and Infertility

T regulatory (Treg) cells are essential mediators of the maternal immune adaptation necessary for embryo implantation. In mice, insufficient Treg cell activity results in implantation failure, or constrains placental function and fetal growth. In women, Treg cell deficiency is linked with unexplained infertility, miscarriage, and pre-eclampsia. To devise strategies to improve Treg cell function, it is essential to define the origin of the Treg cells in gestational tissues, and the regulators that control their functional competence and recruitment. Male seminal fluid is a potent source of the Treg cell-inducing agents TGFβ and prostaglandin E, and coitus is one key factor involved in expanding the pool of inducible Treg cells that react with paternal alloantigens shared by conceptus tissues. In mice, coitus initiates a sequence of events whereby female dendritic cells cross-present seminal fluid antigens and activate T cells, which in turn circulate via the blood to be sequestered into the endometrium. Similar events may occur in the human genital tract, where seminal fluid induces immune cell changes that appear competent to prime Treg cells. Improved understanding of how seminal fluid influences Treg cells in women should ultimately assist in the development of new therapies for immune-mediated pathologies of pregnancy.

Topics: Abortion, Spontaneous; Animals; Dendritic Cells; Embryo Implantation; Endometrium; Female; Humans; Infertility; Isoantigens; Male; Mice; Pre-Eclampsia; Pregnancy; Pregnancy Complications; Prostaglandins E; Semen; Seminal Plasma Proteins; T-Lymphocytes, Regulatory; Transforming Growth Factor beta

Our understanding of reproduction and early embryonic development has directly enabled our manipulation of the mouse genome for tests of gene function in vivo. In this review, we reflect on the 30 years of work that followed this singular accomplishment. We profile murine models that have given us memorable insights into fundamental processes of male and female gametogenesis and the earliest phases of embryonic life reliant on oocyte-transmitted maternal gene products. We highlight intercellular endocrine and paracrine communications essential to gamete development as well as mechanisms essential for passing the genome, with integrity and appropriate epigenetic marks, on to the next generation. Finally, we reflect on the future of reproductive biology: how advances in clinical genetics will provide special opportunities to understand which reproductive processes are affected by genetic lesions and which may allow mutations to originate.

Topics: Adult; Animals; Chromosomes, Human, Y; Embryonic Development; Female; Genetic Techniques; Genetics; Germ Cells; Humans; Infertility; Male; Mice; Mice, Transgenic; Pregnancy; Reproduction; Signal Transduction; Transforming Growth Factor beta

To evaluate the relationship between the size of endometrioma and serum Anti-mullerian hormone (AMH).. A Descriptive study.. This study was conducted at the Bagcilar Training and Research Hospital, Istanbul, Turkey, from January 2015 to January 2020.. Healthy women of reproductive age, who were found to have unilateral endometrioma in ultrasonography, were included in the study group. There were 82 female patients with unilateral endometrioma in the study group and 96 healthy female patients with male factor infertility in the control group. Women with autoimmune disease, a history of pelvic infection or surgery, polycystic ovary syndrome, pregnancy, those undergoing infertility treatment, family history of premature ovarian failure, and those with atypical or suspected endometrioma were excluded. Age, gravida, serum AMH value, and endometrioma size of the study and control groups were recorded. In addition, the endometrioma group was divided into 2 groups with a cut-off size of greater or less than 40 mm. AMH values ​​were evaluated in these two groups.. AMH values ​​of women with endometrioma were significantly lower than the control group (2.03 ng/ml and 3.87 ng/ml, respectively, p<0.001). When the relationship between endometrioma size (greater than 40 mm and less than 40 mm) and AMH was examined, no statistically significant difference was found among serum AMH values (1.89 ng/ml and 2.07 ng/ml, respectively, p=0.65).. The presence of endometrioma was associated with lower AMH suggesting lower ovarian reserve, but endometrioma size was not associated with significant difference in the AMH values.. Endometrioma, AMH, Ovarian reserve, Endometrioma size.

Topics: Anti-Mullerian Hormone; Endometriosis; Female; Humans; Infertility; Male; Polycystic Ovary Syndrome; Pregnancy; Transforming Growth Factor beta

Topics: Animals; Endometrial Neoplasms; Female; Humans; Infertility; Mice; Signal Transduction; Smad2 Protein; Smad3 Protein; Transforming Growth Factor beta