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给予雏鸡地塞米松（Dex）10mg～75mg／kg后24h，诱导脾淋巴细胞产生IL－2和IFN诱生的活性，T、B细胞对Con-A的反应性，以及免疫器官（脾脏、胸腺及法氏囊）重量与体重比值均降低（p＜0．01）。用50mg／kg的RU486阻断GR后，对Dex诱导的免疫抑制无明显地逆转作用，表现为阻断GR后，给予（10～75）mg／kg的Dex24h，上述免疫参数仍明显低于正常雏鸡（P＜0．01），与只给予Dex的雏鸡相比较，无明显差异（P＞0．05）。用25mg／kg的RU486阻断GR，对Dex诱导的免疫抑制作用具有明显地逆转作用，阻断GR后再给予（10～75）mg／kg的Dex后24h，上述免疫参数明显高于只给予Dex的雏鸡（P＜0．01）。若给予10mg／kg或25mg／kg的Dex时，上述免疫参数接近正常水平，表明Dex对雏鸡的免疫抑制作用主要由GR所介导，给予适当量的RU486阻断GR的功能，有利于雏鸡抵抗糖皮质激素诱导的免疫抑制作用。
Induction of IL-2 and IFN-induced activity by splenic lymphocytes, reactivity of T and B cells to Con-A, and immune organs (spleen, thymus) were induced after dexamethasone (Dex) 10 mg to 75 mg / And bursal) weight and body weight ratio decreased (p <0.01). Immunosuppression induced by Dex was not significantly reversed after GR was blocked with RU486 at 50 mg / kg, which was demonstrated by Dex 24h (10-75) mg / kg after blocking GR, and the above immune parameters were still significantly lower than normal There was no significant difference (P> 0.05) between chickens (P <0.01) and chicks fed Dex alone. Blockade of GR with RU486 at 25 mg / kg significantly reversed the dextran-induced immunosuppression. After 24 h treatment of Dex (10-75 mg / kg), the above-mentioned immune parameters were significantly higher than those given only Dex chicks (P <0.01). These immunological parameters approached normal levels at 10 mg / kg or 25 mg / kg of Dex, indicating that the immunosuppressive effect of Dex on chickens is mainly mediated by GR. The appropriate amount of RU486 blocks the function of GR, which is good for chick resistance Glucocorticoid-induced immunosuppression.