Triglia D, Rothenberg E
J Immunol. 1981 Jul;127(1):64-8.
Dexamethasone, administered in vitro either continuously or for a 30-min pulse period followed by a chase of 18 to 24 hr, is shown to decrease protein synthetic rates as well as cellular viabilities in a dose-dependent manner in murine thymocytes. Differential effects on cortical and medullary thymocyte subpopulations should be detectable by alterations in the rates of synthesis of specific molecules which are stable in vitro, relative to total protein synthesis, in the absence of steroids. However, terminal deoxynucleotidyl transferase (TdT), a marker for cortical cells, and Qa-1 and H-2, preferentially expressed in medullary cells, continue to be produced as constant fractions of total synthesis even after treatment with up to 10(-6) M dexamethasone. Furthermore, thymocytes obtained from normal and in vivo cortisone-treated mice show little, if any, difference in their intrinsic sensitivities to dexamethasone in vitro. The results reported here suggest that a corticoresistant thymocyte per se does not exist in vitro and that the thymus may produce factor(S) in vivo that protect the medullary subpopulation from in vivo glucocorticoid-induced lysis.
在体外持续给予地塞米松，或给予30分钟脉冲期后再进行18至24小时的追踪观察，结果显示，地塞米松在小鼠胸腺细胞中以剂量依赖的方式降低蛋白质合成速率以及细胞活力。相对于在无类固醇情况下的总蛋白质合成，通过体外稳定的特定分子合成速率的改变，应该能够检测到对皮质和髓质胸腺细胞亚群的不同影响。然而，即使在用高达10^(-6) M地塞米松处理后，作为总合成恒定比例的末端脱氧核苷酸转移酶（TdT）（皮质细胞的标志物）以及优先在髓质细胞中表达的Qa-1和H-2仍继续产生。此外，从正常小鼠和体内经可的松处理的小鼠获得的胸腺细胞在体外对 地塞米松的内在敏感性几乎没有差异（如果有差异也很小）。此处报道的结果表明，体外不存在本身对地塞米松有抗性的胸腺细胞，并且胸腺可能在体内产生因子，保护髓质亚群免受体内糖皮质激素诱导的裂解。
