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The placenta is one of the few non-hematopoietic tissues to express granulocyte colony stimulation factor (G-CSF). Placental G-CSF production is considered to be one of the major causes of granulocytosis during pregnancy although its physiological role in pregnancy has not yet been examined.The effects of G-CSF on interleukin (IL)-2 and/or IL-12 induced interferon (IFN)-gamma production of magnetic cell sorting (MACS) sorted decidual lymphocytes was examined by enzyme-linked immunosorbent spot-forming cell assay (ELISPOT). The effect of G-CSF on cytotoxicity of decidual lymphocytes against the choriocarcinoma cell line JEG-3 was examined by lactate dehydrogenase (LDH) release assay.As previously reported by us, IL-2 and/or IL-12 activated decidual mononuclear cells were capable of killing choriocarcinoma cells. We observed that G-CSF abolished IFN-gamma production and cytotoxicity of decidual mononuclear cells and MACS sorted CD56+ cells.In addition to its well-known trophic effects on hematopoiesis, our results suggest about new roles of G-CSF in reproductive immunology.

Human endometrial glands contain the highest levels of cyclooxygenase (COX), although whether it is COX-1 and/or COX-2 has not been previously determined. Overexpression of COX-2 may result in the pathogenesis of endometriosis.Tissue sections were obtained from 28 premenopausal women undergoing laparotomy or laparoscopic surgery for benign conditions. Endometrium, ectopic endometriosis tissue and peritoneum were obtained at the time of surgery. Informed consents were obtained from all the patients participating in this study. Immunohistochemistry was performed on consecutive sections of paraffin-embedded tissue using anti-COX-2 antibody. Expressions of COX-2 mRNA in endometrium, ectopic endometriosis tissue, and peritoneum were quantitavely determined by competitive reverse transcription-polymerase chain reaction (RT-PCR).In the uterus, COX-2 was localized in the endometrial epithelium. Eutopic endometrial surface epithelium contains more COX-2 than does glandular epithelium. We observed more frequent and denser COX-2 staining in the ectopic endometriosis implants when compared with eutopic endometrium. Level of COX-2 mRNA in endometriosis was increased up to five times that of eutopic endometria.Hyper activation of COX-2 with abnormal prostaglandin generation is considered to contribute to the pathophysiology of endometriosis and disease progression.