Immunology: Bone marrow-derived cell populations in uterine and ectopic endometrium

Fernández-Shaw, S.; Clarke, M T; Hicks, B.R.; Naish, Caroline; Barlow, David H.; Starkey, Phyllis M.

doi:10.1093/oxfordjournals.humrep.a136286

Cited by 32 publications

(14 citation statements)

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“…However, other studies have reported no difference between the patients suffering from recurrent pregnancy loss and fertile patients Likewise, the data from studies examining uNK cells in patients with endometriosis are also variable. Some laboratories have reported a lower percentage of CD56 + NK cells and a defect in NK activity in the eutopic endometrium of women with endometriosis . Studies from our laboratory did not observe a difference in the percentage of CD56+ uNK cells when comparing patients with endometriosis to healthy controls.…”

Section: Differences In Uterine Nk Cells Associated With Implantationcontrasting

confidence: 49%

Uterine Leukocyte Function and Dysfunction: A Hypothesis on the Impact of Endometriosis

Parkin

Fazleabas

2016

American J Rep Immunol

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Endometriosis is a chronic inflammatory disease characterized by the growth of endometrial glands and stroma outside of the uterus. The disease affects approximately 10–15% of women of reproductive age and presents with clinical symptoms of pelvic pain and infertility. Changes in the leukocyte populations within the ectopic tissue and eutopic endometrium have been reported, and data suggest these alterations contribute to the pathology and symptoms of the disease. In this review, we discussed differences when comparing uterine NK cells and regulatory T cells within the eutopic endometrium between patients with endometriosis and healthy patients, and how these differences relate to implantation failure and/or decreased clearance of menstrual tissue in patients with the disease. The data demonstrate a critical need to examine endometrium and menstrual tissue in patients with endometriosis excluded from studies examining unknown causes of infertility and heavy menstrual bleeding. The information gathered from excluded patients will further enhance our understanding of how the immune system contributes to the pathophysiology of endometriosis and help to identify biomarkers for patients at higher risk for developing endometriosis‐associated infertility.

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Section: Differences In Uterine Nk Cells Associated With Implantationcontrasting

confidence: 49%

Uterine Leukocyte Function and Dysfunction: A Hypothesis on the Impact of Endometriosis

Parkin

Fazleabas

2016

American J Rep Immunol

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“…T lymphocyte is one of two major leukocyte subpopulations in endometriotic tissues along with macrophage 27 . The number of total T lymphocytes as well as that of activated T lymphocytes was shown to be increased in ectopic endometrium compared to eutopic endometrium, 28,29 whereas one study failed to detect any differences 30 . As a specific subgroup of T lymphocytes, gamma delta T lymphocytes were demonstrated in the stroma of endometriotic tissues, although its function remains to be elucidated 31 …”

Section: T Lymphocytesmentioning

confidence: 99%

Lymphocytes in Endometriosis

Osuga

Koga

Hirota

et al. 2010

American Journal of Reproductive Immunology

147

107

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Endometriosis is a disease characterized by the presence of endometriotic tissue outside the uterine cavity. Although its pathogenesis remains to be elucidated, immune status is suggested to play an important role in the initiation and the progression of the disease. In particular, immune cells in lymphoid lineage that comprised T and B lymphocytes and natural killer cells play essential roles in determining either accept or reject survival, implantation, and proliferation of endometrial and endometriotic cells. Numerous studies have shown aberrant functions of these immune cells in women with endometriosis. The abnormalities include reduced activity of cytotoxic T cells and NK cells, cytokine secretion by helper T cells, and autoantibody production by B lymphocytes. These alterations are suggested to be induced by various manners and promote the disease. Understanding of these immune aspects in endometriosis is thus expected to benefit the treatment of the disease.

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“…The similar findings were pointed out by several publications. 36,37 Tie-2 expressing BM-derived EPCs need vasculogenic environments introduced by angiogenic cytokines secreted from BM-derived macrophages. Therefore, this balance of EPCs and macrophages might play a pivotal role in neovascularization in endometrial formation.…”

Section: Masuda Et Al Estrogen and Endothelial Progenitor Cellsmentioning

confidence: 99%

Estrogen-Mediated Endothelial Progenitor Cell Biology and Kinetics For Physiological Postnatal Vasculogenesis

Masuda

Kalka

Takahashi

et al. 2007

Circulation Research

149

106

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Abstract-Estrogen has been demonstrated to promote therapeutic reendothelialization after vascular injury by bone marrow (BM)-derived endothelial progenitor cell (EPC) mobilization and phenotypic modulation. We investigated the primary hypothesis that estrogen regulates physiological postnatal vasculogenesis by modulating bioactivity of BMderived EPCs through the estrogen receptor (ER), in cyclic hormonally regulated endometrial neovascularization. Cultured human EPCs from peripheral blood mononuclear cells (PB-MNCs) disclosed consistent gene expression of ER ␣ as well as downregulated gene expressions of ER ␤. Under the physiological concentrations of estrogen (17␤-estradiol, E2), proliferation and migration were stimulated, whereas apoptosis was inhibited on day 7 cultured EPCs. These estrogen-induced activities were blocked by the receptor antagonist, ICI182,780 (ICI). In BM transplanted (BMT) mice with ovariectomy (OVX) from transgenic mice overexpressing ␤-galactosidase (lacZ) regulated by an endothelial specific Tie-2 promoter (Tie-2/lacZ/BM), the uterus demonstrated a significant increase in BM-derived EPCs (lacZ expressing cells) incorporated into neovasculatures detected by CD31 immunohistochemistry after E2 administration. The BM-derived EPCs that were incorporated into the uterus dominantly expressed ER ␣, rather than ER ␤ in BMT mice from BM of transgenic mice overexpressing EGFP regulated by Tie-2 promoter with OVX (Tie-2/EGFP/BMT/OVX) by ERs fluorescence immunohistochemistry. An in vitro assay for colony forming activity as well as flow cytometry for CD133, CD34, KDR, and VE-cadherin, using human PB-MNCs at 5 stages of the female menstrual-cycle (early-proliferative, pre-ovulatory, post-ovulatory, mid-luteal, late-luteal), revealed cycle-specific regulation of EPC kinetics. These findings demonstrate that physiological postnatal vasculogenesis involves cyclic, E2-regulated bioactivity of BM-derived EPCs, predominantly through the ER␣. (Circ Res. 2007;101:598-606.)Key Words: estrogen Ⅲ endothelial progenitor cell Ⅲ estrogen receptor Ⅲ physiological postnatal vasculogenesis I n the female reproductive system, neovascularization is a recurring phenomemnon controlled by cyclic development of transient structure and cyclical repair of damaged tissue. 1 The ovarian sex steroid hormones, estrogen and progesterone, are primarily uterotropic and control the cyclical patterns of uterine cell proliferation and vascular growth that occur throughout the nonpregnant menstrual cycle. Given the synchronized nature of neovascularization in this cyclical mannter, it is assumed that angiogenic growth factor expression is induced by steroid hormones and regulates blood vessel formation in reproductive organogenesis. [2][3][4][5] Despite clinical evidence for the significant role of steroid hormones in endometrial neovascularization, further investigation using in vitro and in vivo experiments have yielded inconclusive results regarding pathophysiological mechanisms in angiogenesis. 6 -10 Moreover, estrogen has been sh...

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Immunology: Bone marrow-derived cell populations in uterine and ectopic endometrium

Cited by 32 publications

References 0 publications

Uterine Leukocyte Function and Dysfunction: A Hypothesis on the Impact of Endometriosis

Uterine Leukocyte Function and Dysfunction: A Hypothesis on the Impact of Endometriosis

Lymphocytes in Endometriosis

Estrogen-Mediated Endothelial Progenitor Cell Biology and Kinetics For Physiological Postnatal Vasculogenesis

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