Bradley L M, Mishell R I
Proc Natl Acad Sci U S A. 1981 May;78(5):3155-9. doi: 10.1073/pnas.78.5.3155.
The effects of dexamethasone (Dex) on the functions of antigen-primed helper and suppressor T cells were studied in humoral immune responses in vitro. In doses equivalent to elevated physiologic concentrations, the suppressor T cell activity was abolished. In contrast, the helper T cell function was resistant to even pharmacologic concentrations of Dex. The apparent steroid resistance of the helper T cells was found to be mediated by the products of activated macrophages. While macrophage factors protected helper T cells from steroid inhibition, they did not prevent the effects of Dex on suppressor T cells. Because bacterial cell wall and membrane components are potent inducers of the factors that mediate steroid resistance of helper T cells, the combination of physiologically elevated levels of steroids and macrophage factors during acute infections may function to facilitate the expression of host immunity. However, the persistance of these conditions, as in chronic inflammation, may also contribute to the pathogenesis of autoimmunity by perturbing the balance of immune regulation by helper and suppressor T cells.
在地塞米松（Dex）对体外体液免疫应答中抗原致敏辅助性T细胞和抑制性T细胞功能的影响的研究中，当剂量等同于生理浓度升高时，抑制性T细胞活性被消除。相反，辅助性T细胞功能对甚至是药理浓度的地塞米松都具有抗性。发现辅助性T细胞明显的类固醇抗性是由活化巨噬细胞的产物介导的。虽然巨噬细胞因子保护辅助性T细胞免受类固醇抑制，但它们并不能阻止地塞米松对抑制性T细胞的作用。由于细菌细胞壁和膜成分是介导辅助性T细胞类固醇抗性的因子的有效诱导剂，急性感染期间生理水平升高的类固醇和巨噬细胞因子的组合可能起到促进宿主免疫表达的作用。然而，如在慢性炎症中这些情况的持续存在，也可能通过扰乱辅助性T细胞和抑制性T细胞免疫调节的平衡而导致自身免疫性疾病的发病机制。
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