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甲状腺功能正常的Graves眼病患者自然杀伤细胞活性受抑制。

Suppressed natural killer cell activity in patients with euthyroid Graves' ophthalmopathy.

作者信息

Pedersen B K, Perrild H, Feldt-Rasmussen U, Christensen T, Klarlund K, Hansen J M

机构信息

Department of Medicine F, Gentofte Hospital, Copenhagen, Denmark.

出版信息

Autoimmunity. 1989;2(4):291-8. doi: 10.3109/08916938908997155.

Abstract

The purpose of the present study was to determine whether patients with euthyroid Graves' exophthalmopathy have an impaired NK cell function compared to patients with Graves' hyperthyroidism and healthy controls. The NK cell activity measured against K562 target cells was significantly suppressed (p less than 0.01) in patients with euthyroid Graves' ophthalmopathy, whereas the NK cell activity of patients with Graves' hyperthyroidism was not. Although interferon-alpha, interleukin-2 and indomethacin significantly enhanced (p less than 0.01) the NK cell activity in all three groups, none of these agents fully restored the defective NK cell activity in euthyroid Graves' ophthalmopathy. The concentrations in the blood of large granular lymphocytes and CD16 positive cells did not differ between the three groups, furthermore an immunosuppressive serum factor was not detected. The number of effector/target cell conjugates did not differ between patients and controls, whereas the interferon-alpha induced production of a soluble natural killer cytotoxic factor (NKCF) with specificity for NK sensitive target cells was suppressed in patients with Graves' euthyroid ophthalmopathy. We conclude that one of the mechanisms underlying the defective NK cell activity in patients with euthyroid ophthalmopathy may be an impairment of the release of NKCF from the NK cells.

摘要

本研究的目的是确定与格雷夫斯甲亢患者和健康对照相比,甲状腺功能正常的格雷夫斯突眼症患者的自然杀伤(NK)细胞功能是否受损。与格雷夫斯甲亢患者不同,甲状腺功能正常的格雷夫斯眼病患者针对K562靶细胞测得的NK细胞活性显著受到抑制(p小于0.01)。虽然α干扰素、白细胞介素-2和消炎痛显著增强了(p小于0.01)所有三组的NK细胞活性,但这些药物均未完全恢复甲状腺功能正常的格雷夫斯眼病患者存在缺陷的NK细胞活性。三组之间大颗粒淋巴细胞和CD16阳性细胞的血液浓度没有差异,此外未检测到免疫抑制血清因子。患者和对照之间效应细胞/靶细胞结合物的数量没有差异,而α干扰素诱导的对NK敏感靶细胞具有特异性的可溶性自然杀伤细胞细胞毒性因子(NKCF)的产生在格雷夫斯甲状腺功能正常眼病患者中受到抑制。我们得出结论,甲状腺功能正常的眼病患者NK细胞活性缺陷的潜在机制之一可能是NK细胞释放NKCF受损。

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