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采用荧光标记的抗ＣＤ２５单抗，观察了地塞米松对大鼠脾淋巴细胞表达低亲和力ＩＬ－２受体（ＣＤ２５抗原）的影响。结果显示，在ＣｏｎＡ激活的淋巴细胞培养体系中加入地塞米松后，低亲和力ＩＬ－２受体的表达明显受到抑制；表达ＣＤ２５抗原的阳性细胞率亦明显减少。采用￣（１２５）Ｉ－ｒＩＬ－２结合分析实验，进一步研究了地塞米松对高亲和力ＩＬ－２受体的影响。结果证实，１０ｎｍｏｌ／Ｌ地塞米松使高亲和力ＩＬ－２受体的数量由１０．０±０．７３降至６．５１±１．８２ｆｍｏｌ／１０￣７细胞（ｎ＝４），但亲和力无显著变化。糖皮质激素的上述调节作用可能是其抑制免疫功能的重要分子机制之一。
Fluorescently labeled anti-CD25 mAb was used to observe the effect of dexamethasone on the expression of low affinity IL-2 receptor (CD25 antigen) in rat splenic lymphocytes. The results showed that the low affinity IL-2 receptor expression was significantly inhibited after adding dexamethasone in ConA-activated lymphocyte culture system, and the positive rate of CD25 antigen expression was significantly decreased. The effect of dexamethasone on the high-affinity IL-2 receptor was further studied using a ~ (125) I-rIL-2 binding assay. The results confirmed that 10nmol / L dexamethasone reduced the number of high-affinity IL-2 receptors from 10.0 ± 0.73 to 6.51 ± 1.82fmol / 10-7 cells (n = 4), but with no affinity Significant changes. The above-mentioned regulation of glucocorticoid may be one of the important molecular mechanisms of its inhibition of immune function.