Fuggetta M P, Graziani G, Aquino A, D'Atri S, Bonmassar E
Institute of Experimental Medicine, CNR, Rome, Italy.
Int J Immunopharmacol. 1988;10(6):687-94. doi: 10.1016/0192-0561(88)90022-7.
It is well known that glucocorticoids depress the natural killer (NK) activity of human peripheral blood lymphocytes when used both in vivo and in vitro. Since interferons enhance natural cytotoxicity, potential interaction between beta-interferon and hydrocortisone hemisuccinate has been investigated using mononuclear cells of peripheral blood obtained from 17 healthy donors. At the end of in vitro treatment mononuclear cells were tested for NK activity against K562 cells in a 4 h 51Cr-release assay. The results suggest that beta-interferon at the optimal treatment schedule (i.e. before and after exposure to hydrocortisone) is capable of abrogating the hydrocortisone-mediated impairment of NK function. These findings provide valuable suggestions for optimal treatment schedules with beta-interferon (i.e. beta-interferon treatment before and after exposure of effector cells to hydrocortisone) for overriding the suppressive effects of glucocorticoid therapy on natural immunity.
众所周知,糖皮质激素在体内和体外使用时都会抑制人外周血淋巴细胞的自然杀伤(NK)活性。由于干扰素可增强自然细胞毒性,因此已使用从17名健康供体获得的外周血单个核细胞研究了β-干扰素与氢化可的松半琥珀酸酯之间的潜在相互作用。在体外处理结束时,在4小时51Cr释放试验中测试单个核细胞对K562细胞的NK活性。结果表明,在最佳治疗方案下(即在暴露于氢化可的松之前和之后)的β-干扰素能够消除氢化可的松介导的NK功能损害。这些发现为使用β-干扰素的最佳治疗方案(即效应细胞暴露于氢化可的松之前和之后进行β-干扰素治疗)提供了有价值的建议,以克服糖皮质激素疗法对自然免疫的抑制作用。