Expression of Inhibitory‐Motif Killer Immunoglobulin‐Like Receptor, KIR2DL1, is Increased in Natural Killer Cells from Women with Pelvic Endometriosis

Abstract

ITIM-KIR expressing NK cells might confer tolerance to peritoneal endometriotic implants.

Natural Killer Receptors on CD8 T Cells and Natural Killer Cells from Different HLA-C Phenotypes in Melanoma Patients

“…These facts, such as it has been recently proposed for endometriosis, suggest that CD56 NK cells Table 4. HLA-C alleles and phenotypes in melanoma patients and controls positive for KIR2DL1/S1 might contribute to the induction of tolerance against melanoma (45). Moreover, these findings might support the observation of Guillot et al (46), about the absence of a link between the effect of IFN-a on perforin expression in cytotoxic cells and the posttherapeutic disease evolution, because the expression of KIR receptors on cytotoxic NK cell surface could, at least partially, block the antitumoral function of NK cells.…”

IL15 promotes growth and invasion of endometrial stromal cells and inhibits killing activity of NK cells in endometriosis

“…It has been proven that the number of peripheral blood and abdominal NK cells in EMS patients has no significant difference ( Oosterlynck et al 1994, Matsuoka et al 2005. However, the activity visibly weakens, and the impaired degree of NK cell activity positively correlates with EMS development.…”

Role of NK Cells in Endometriosis

“…This suggests that KIRs expressed on NK cells can respond to their HLA class I ligands on eutopic endometrium [39][40][41]. It was also reported that progesterone induces HLA class I mRNA expression by cultured cells from secretory endometrium [51].…”

“…In women with endometriosis, expression of inhibitory killer immunoglobulin-like receptors on NK cells from PB and PF is significantly upregulated compared with the level of expression in women without endometriosis [39][40][41], indicating a decrease of NK cell activity and cytotoxicity for endometriotic cells.…”

“…Our investigations have suggested that HLA-C-expressing endometrial cells may enter the peritoneal cavity via retrograde menstruation and react with peritoneal NK cells expressing KIR2DL1 [39][40][41]. Impaired KIR2DL1 expression by peritoneal NK cells could allow endometrial cells to survive in the peritoneal cavity and undergo ectopic implantation, favoring the onset and progression of endometriosis.…”