Moynihan J A, Callahan T A, Kelley S P, Campbell L M
Department of Psychiatry, University of Rochester Medical Center, New York 14642, USA.
Cell Immunol. 1998 Feb 25;184(1):58-64. doi: 10.1006/cimm.1998.1259.
Our previous work has documented that physical or psychological stress can alter interleukin (IL)-2, IL-4, and interferon (IFN)-gamma production by spleen or lymph node cells in vitro. To determine if adrenal hormones might be mediating these stress-induced changes in type 1 and type 2 cytokines and immune effector functions, we cultured spleen cells in vitro with either the synthetic glucocorticoid dexamethasone (DEX) or the putative restorative hormone dehydroepiandrosterone (DHEA). Spleen cells were obtained from either young (5-6 weeks old) or mature (7-8 months old) BALB/c mice that were either unimmunized or immunized with the T-cell-dependent antigen keyhole limpet hemocyanin (KLH). We determined that DEX suppressed production of all three cytokines examined. DHEA was not associated with any enhancement of cytokine production. These data challenge the hypothesis that glucocorticoids can differentially regulate Th1-like versus Th2-like cytokine production. Further, they suggest that in stress paradigms in which differential regulation of cytokine production and effector function has been observed, other neuroendocrine factors in addition to glucocorticoids must be relevant.
我们之前的研究记录表明,身体或心理应激能够在体外改变脾脏或淋巴结细胞产生白细胞介素(IL)-2、IL-4和干扰素(IFN)-γ的情况。为了确定肾上腺激素是否可能介导这些应激诱导的1型和2型细胞因子变化及免疫效应功能,我们在体外将脾细胞与合成糖皮质激素地塞米松(DEX)或假定的恢复性激素脱氢表雄酮(DHEA)一起培养。脾细胞取自未免疫或用T细胞依赖性抗原血蓝蛋白(KLH)免疫的年轻(5 - 6周龄)或成熟(7 - 8月龄)BALB/c小鼠。我们确定DEX抑制了所检测的所有三种细胞因子的产生。DHEA与细胞因子产生的任何增强均无关。这些数据对糖皮质激素可差异调节Th1样与Th2样细胞因子产生这一假说提出了挑战。此外,它们表明,在已观察到细胞因子产生和效应功能存在差异调节的应激模式中,除糖皮质激素外的其他神经内分泌因子必定也与之相关。