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Role of NK Cells in Endometriosis

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Endometriosis

Abstract

Impaired natural killer (NK) cell activity in women with endometriosis is thought to promote implantation and the progressive growth of endometrial tissue in accordance with Sampson’s hypothesis. However, the mechanisms responsible for decreased NK cell activity and the antigens recognized by NK cells in these women are not clear.

Decreased NK cell activity in the peripheral blood (PB) and peritoneal fluid (PF) of women with endometriosis was first reported by Oosterlynck et al. and subsequent investigators have identified the depression of NK cell function in women with this disorder. Decreased NK cell activity in women with endometriosis is thought to allow the implantation of endometrial tissue in the manner of a graft, but the mechanisms underlying the decline of NK cell activity remain uncertain.

We focused on the expression of HLA-G, a ligand of NK cell receptors, and its changes in eutopic endometrium during the menstrual cycle. HLA-G expression was only identified in eutopic endometrium during the menstrual phase, but not during the proliferative or secretory phases. HLA-G-expressing cells were also detected in peritoneal fluid during the menstrual phase.

Retrograde menstruation may allow HLA-G-expressing endometrial tissue to enter the peritoneal cavity, where it should be scavenged by the immune surveillance system. Because peritoneal NK cells play an important role in this system, impairment of their cytotoxicity via HLA-G could allow the survival and implantation of peritoneal endometrial cells.

In this article, we discuss the pathogenesis of endometriosis from the perspective of intraperitoneal interactions between NK cell receptors and their ligands (antigens) that enter the peritoneal cavity on cells shed from eutopic endometrium via retrograde menstruation.

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Maeda, N. (2014). Role of NK Cells in Endometriosis. In: Harada, T. (eds) Endometriosis. Springer, Tokyo. https://doi.org/10.1007/978-4-431-54421-0_5

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  • DOI: https://doi.org/10.1007/978-4-431-54421-0_5

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