Decreased Natural Killer Cell Activity in Women with Endometriosis

Tanaka, Eiichi; Sendo, Fujiro; Kawagoe, Shinnosuke; Hiroi, Masahiko

doi:10.1159/000292720

Cited by 67 publications

(44 citation statements)

References 12 publications

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“…In addition, we demonstrated that treatments with antide and TNF-SHARC increased NK cell activity similar to the human studies (Umesaki et al, 1999). Clinical data show reduced NK cell activity in women with endometriosis (Tanaka et al, 1992;Quaranta et al, 2006), which correlates with the severity of the disease (Wilson et al, 1994). Recent studies propose the decreased NK cell activity in women with endometriosis could be due to an increased proportion of NK cells expressing CD94/NKG2A (Galandrini et al, 2008).…”

Section: Discussionsupporting

confidence: 72%

A Long-Acting Tumor Necrosis Factor α-Binding Protein Demonstrates Activity in Both In Vitro and In Vivo Models of Endometriosis

Altan¹,

Denis²,

Kagan³

et al. 2010

J Pharmacol Exp Ther

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Endometriosis is characterized by the presence of elevated proinflammatory cytokines such as tumor necrosis factor (TNF) ␣ in the peritoneal cavity. Blocking interaction of TNF␣ with its receptor by the addition of excess TNF␣-binding protein (TBP)-1 (a soluble form of TNF receptor-1) was effective in animal models of endometriosis. Recently, a novel, high-affinity inhibitor of TNF␣, TNF-soluble high-affinity receptor complex (TNF-SHARC), was created by fusing TBP to both the ␣ and ␤ subunits of inactive human chorionic gonadotropin. This dimeric protein was effective in inhibiting collagen-induced arthritis in mice. In the present study, the efficacy of TNF-SHARC in cellular and in vivo models of endometriosis was examined. TBP and TNF-SHARC dose-dependently inhibited TNF␣-induced secretion of interleukin (IL)-6, IL-8, granulocyte macrophage-colony-

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Section: Discussionsupporting

confidence: 72%

A Long-Acting Tumor Necrosis Factor α-Binding Protein Demonstrates Activity in Both In Vitro and In Vivo Models of Endometriosis

Altan¹,

Denis²,

Kagan³

et al. 2010

J Pharmacol Exp Ther

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“…The pathogenesis of endometriosis is not well understood. Several reports, Recombinant IL-2, U/ml We confirmed this defect, and with in vitro depletion of natural killer (NK) cells, using the anti-Leu-llb mono clonal antibody, we showed that NK cells were responsi ble for the in vitro killing of endometrial cells [2], Next, women with endometriosis had a decreased NK activity in peripheral blood [2], This was confirmed by several investigators [3][4][5][6],…”

Section: Introductionsupporting

confidence: 68%

“…The age range for the women with endometriosis was 22-39 years with a median o f 29.1, and for the women without endometrio sis it was 2 6 -4 4 years with a median o f 30. 4.…”

Section: Patientsmentioning

confidence: 99%

Lymphokine-Activated Killer Activity in Women with Endometriosis

Oosterlynck

Lacquet²,

Waer³

et al. 1994

Gynecol Obstet Invest

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The aim of the present study was to investigate whether women with endometriosis displayed a decreased lymphokine-activated killer (LAK) activity. In 15 women with and 7 women without endometriosis the cytotoxicity against four different tumor cell lines – K562, the endometrium carcinomas AN3CA and RL95, the natural-killer (NK)-resistant Daudi cell line – was investigated, using either freshly isolated peripheral blood mononuclear cells (PBMC) or recombinant interleukin (IL)-2-stimulated PBMC. In 5 additional women collagenase-DNase-digested endometrium was used, to investigate whether recombinant IL-2-activated lymphocytes displayed an increased cytotoxicity against fresh and cultured endometrial cells. The cytotoxicity of unstimulated PBMC toward K562, AN3CA and RL95 target cells was decreased in women with endometriosis compared to women without endometriosis (p < 0.05, for all). After recombinant IL-2 stimulation the cytotoxicity toward the four different target cells increased significantly, both in women with and without endometriosis. There was no difference in LAK-mediated cytotoxicity against the four tumoral cells between women with and without endometriosis. Significant LAK activity was demonstrated against both fresh and cultured (72 h) endometrial cells. The cytotoxicity of autologous lymphocytes against cultured endometrial cells was 31.0+ 17 versus 67.4 ± 5.8%, using lymphocytes cultured in medium without and with recombinant IL-2, respectively (paired t test, p < 0.02). These results demonstrated that the decreased NK activity in peripheral blood of women with endometriosis was corrected after in vitro recombinant IL-2 stimulation of lymphocytes. Furthermore, this study showed that cytotoxicity toward fresh and cultured endometrial cells increased after in vitro incubation of PBMC with recombinant IL-2.

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“…The pathogenesis of endometriosis, however, is also found to be associated with a derangement of the immune system, and especially with a decreased clearance of peritoneal fluid endometrial cells as a result of decreased cytotoxic T and natural killer (NK) cell activity. [2][3][4][5][6] A variety of inflammatory cytokines, such as interleukin-1, tumour necrosis factor-a, and interferon-c (IFN-c), have been reported to play important roles in endometriosis. [6][7][8][9] Among them, IFN-c is a multifunctional cytokine mainly secreted by T helper type-1 (Th1) cells and NK cells.…”

Section: Introductionmentioning

confidence: 99%