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Problem: NK-cell dysfunction in endometriosis is suggested to contribute to the survival of ectopic endometrial tissue. However, the underlying causes of this impairment remain unclear. NK cells are divided into: CD56+bright, which produce high amounts of cytokines but have low or no cytotoxic ability, and CD56+dim, which are mainly cytotoxic. CD56+bright NK cells, constitutively present in human endometrium (eNK cells), represent only 0–2% of NK cells in PBMC, where CD56+dim cells dominate.

Method of Study: NK-cell subpopulations and NKG2D receptor expression in PBMC were analyzed by flow cytometry in two cohorts of untreated and treated endometriosis patients and healthy age-matched controls.

Results: Elevated numbers of CD56+bright cells were observed in 8 of 21 untreated endometriosis patients compared to controls. These numbers were normalized following surgery and hormonal treatment. The NKG2D receptor expression was reduced in untreated patients compared to controls and treated patients.

Conclusions: The significantly increased proportion of peripheral CD56+brightNK/eNK cells may result from migration of these cells from ectopic endometrial tissue. The downregulation of NKG2D receptor expression in PBMCs may be mediated by immunosuppressive endometriotic exosomes, as previously reported by us. Taken together, our results suggest that: (1) the impaired NK cell cytotoxicity in untreated endometriosis patients may be due both to an influx of CD56+bright/eNK cells and exosome-induced NKG2D receptor downregulation; and (2) elevated numbers of peripheral CD56+bright NK cells could be considered as a potential diagnostic marker for endometriosis.