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Uterine natural killer (uNK) cells are a specialized subset of innate lymphoid cells that constitute the most abundant leukocyte population in the human decidua during early pregnancy (Moffett & Colucci, 2014). Distinct from peripheral blood NK cells, uNK cells are predominantly CD56bright CD16- and exhibit low cytotoxicity, instead serving as critical regulators of the maternal-fetal interface (Bulmer et al., 2010). Their primary biological roles include the secretion of pro-angiogenic factors like vascular endothelial growth factor (VEGF) and placental growth factor (PLGF), which facilitate the remodeling of maternal spiral arteries and the regulation of extravillous trophoblast invasion (Lash et al., 2010). Dysregulation in the number or activation state of these cells has been linked to various reproductive complications, including recurrent pregnancy loss, pre-eclampsia, and unexplained infertility (Tang et al., 2011). Therapeutic interventions such as corticosteroids (e.g., prednisolone) and intravenous immunoglobulins are often employed in clinical settings to modulate uNK cell activity, although their use remains a subject of debate due to the need for more robust clinical trial evidence (Cooper et al., 2016).
Pharmacological modulation of uterine natural killer cell density, phenotype, and cytokine secretion to promote an environment conducive to embryo implantation and placental development (Quenby et al., 2005; Winger et al., 2011).
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