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Glycodelin-A as a paracrine regulator in early pregnancy

Lee, Cheuk-Lun and Lam, Kevin KW and Koistinen, Hannu and Seppala, Markku and Kurpisz, Maciej and Fernandez, Nelson and Pang, Ronald TK and Yeung, William SB and Chiu, Philip CN (2011) Glycodelin-A as a paracrine regulator in early pregnancy. In: UNSPECIFIED, ? - ?, Ireland.

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Glycodelin-A (GdA) is a glycoprotein secreted from the endometrial glands and decidual glandular epithelium. Given its abundance and ubiquitous distribution in the first trimester uterus, GdA may be involved in early placental development via its modulatory effect on immune and trophoblast cells. GdA inhibits activation and proliferation, and induces apoptosis of T cells. By selectively inducing Th1 cell death, GdA may shift the Th1/Th2 ratio at the feto-maternal interface. This is also achieved indirectly through enhanced expression of Fas in the Th1 cells, thus making them vulnerable to cell death through Fas ligand expressed on trophoblast, endometrial, and activated T helper cells. GdA also promotes secretion of the Th2 cytokines IL-6 and IL-13 from NK cells, and induces immunological tolerance of dendritic cells and apoptosis of monocytes. Specific glycosylation is a prerequisite for the biological activities of GdA. Reduction in α2-6 sialylation of GdA, as in gestational diabetes, is associated with impairment of its T cell apoptosis-inducing activities. This review integrates recent studies on GdA and its role as a paracrine regulator in early pregnancy. © 2011 Elsevier Ireland Ltd.

Item Type: Conference or Workshop Item (UNSPECIFIED)
Additional Information: Published proceedings: Journal of Reproductive Immunology
Uncontrolled Keywords: Glycodelin-A; Placentation; Fetal tolerance; Glycosylation; Immunoendocrinology
Subjects: Q Science > QH Natural history > QH301 Biology
Divisions: Faculty of Science and Health
Faculty of Science and Health > Life Sciences, School of
SWORD Depositor: Elements
Depositing User: Elements
Date Deposited: 06 Oct 2011 14:53
Last Modified: 18 Aug 2022 11:00

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