Randazzo B, Hirschberg T, Hirschberg H
Int J Immunopharmacol. 1984;6(5):419-23. doi: 10.1016/0192-0561(84)90079-1.
A mechanism by which the steroid methylprednisolone inhibits the T cell proliferation normally seen in antigen driven cultures was investigated. At methylprednisolone concentrations less than 10 micrograms ml-1 inhibition of cellular proliferation was almost exclusively via the inhibition of the production of interleukin-2 by activated T cells. The steroid seemed to inhibit IL-2 production directly and not via reduced sensitivity to interleukin-1 by IL-2 producer T cells, or reduced IL-1 production by the antigen presenting monocytes. At methylprednisolone concentrations of greater than 10 micrograms ml-1 direct inhibition of the T cell receptor to antigen complexes presented by cooperating monocytes seemed the most likely explanation. T cells in the presence of antigen and monocytes and MP concentrations of greater than 10 micrograms ml-1 did not produce IL-2 and were incapable of expressing IL-2 receptors. The inhibiting effects of methylprednisolone therefore are via several mechanisms depending on the concentration of the steroid employed.
研究了类固醇甲泼尼龙抑制抗原驱动培养中正常出现的T细胞增殖的机制。在甲泼尼龙浓度低于10微克/毫升时，细胞增殖的抑制几乎完全是通过抑制活化T细胞产生白细胞介素-2实现的。该类固醇似乎直接抑制白细胞介素-2的产生，而不是通过白细胞介素-2产生T细胞对白细胞介素-1敏感性降低，或抗原呈递单核细胞产生白细胞介素-1减少来实现。在甲泼尼龙浓度大于10微克/毫升时，最可能的解释似乎是T细胞受体对协同单核细胞呈递的抗原复合物的直接抑制。在存在抗原、单核细胞且甲泼尼龙浓度大于10微克/毫升的情况下，T细胞不产生白细胞介素-2，并且无法表达白细胞介素-2受体。因此，甲泼尼龙的抑制作用取决于所使用类固醇的浓度，通过几种机制发挥作用。
