Platelet-derived TGF-β1 mediates the down-modulation of NKG2D expression and may be responsible for impaired natural killer (NK) cytotoxicity in women with endometriosis

摘要: STUDY QUESTION Does platelet-derived transforming growth factor-β1 (TGF-β1) have any role in the reduced cytotoxicity of natural killer (NK) cells women with endometriosis? SUMMARY ANSWER Platelet-derived TGF-β1 suppresses expression NK Group 2, Member D (NKG2D) on cells, resulting endometriosis, but neutralization reverses reduction. WHAT IS KNOWN ALREADY are cytotoxic lymphocytes that play an important peritoneal immune surveillance, and their function is known to be impaired endometriosis. There increased platelet aggregation endometriotic lesions activation rate peripheral blood yet activated platelets release copiousTGF-β1, which a potent immunosuppressive molecule cell NKG2D expression. DESIGN, SIZE, DURATION Cross-sectional clinical studies 30 endometriosis 33 without vitro experimentation blockade. PARTICIPANTS/MATERIALS, SETTING, METHODS Peritoneal fluid (PF) samples from premenopausal age- menstrual phase-matched controls were collected. Platelet count, white (WBC) mean volume (MPV), rate, concentration, levels PF evaluated. The apoptosis freshly isolated treated presence or absence anti-TGF-β1 antibody also determined. MAIN RESULTS AND THE ROLE OF CHANCE WBC MPV, concentration significantly elevated when compared those correlated positively (r = 0.59, P < 0.01), suggesting responsible, at least part, for concentration. Both negatively -0.36, 0.01, r -0.45, respectively). In addition, level found if co-cultured blockade effectively LIMITATIONS, REASONS FOR CAUTION This study limited by cross-sectional nature study. WIDER IMPLICATIONS FINDINGS potently activate so it even overrides inhibitory signals transduced other receptors. first time we demonstrate may responsible as well provides another piece evidence critical roles development anti-platelet treatment should improve functionality treating Equally important, this highlights lesion microenvironment shaping cell-mediated anti-endometriotic immunity. FUNDING/COMPETING INTERESTS research was supported part grants 81270676 (S.-W.G.), 81471434 81530040 81370695 (X.L.) National Natural Science Foundation China, grant 2013ZYJB0019 Shanghai Municipal Commission Health Family Planning. None authors has anything disclose.