Cytokines, acute-phase proteins, and hormones -: IL-1 and TNF-α production in contact-mediated activation of monocytes by T lymphocytes
Cytokines, acute-phase proteins, and hormones -: IL-1 and TNF-α production in contact-mediated activation of monocytes by T lymphocytes
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DOI：
10.1111/j.1749-6632.2002.tb04248.x
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发表时间：
2002-01-01
期刊：
影响因子：
--
通讯作者：
Dayer, JM
中科院分区：
文献类型：
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作者：
Burger, D;Dayer, JM
细胞因子网络是一个动态平衡系统，必须以类似于酸/碱平衡的方式来感知。生物液中任何细胞因子的水平只有考虑到其他协同作用的细胞因子的水平，以及它们各自的抑制剂的水平，才能正确解释。以及每一种细胞因子受体。由于它们在许多不同的过程(包括细胞生长和分化、发育和修复过程中导致体内平衡的恢复)具有很强的活性，因此细胞因子的活性必须受到自然抑制机制的严格控制。由于细胞因子的主要功能之一是调节免疫和炎症系统之间的相互作用，因此人们认为慢性免疫性炎症性疾病的部分原因可能是细胞因子的不受控制的产生。根据炎症的阶段或确定的生物效应，相同的细胞因子可能是促炎的，也可能是抗炎的。例如，这适用于IL-4、IL-10和TGFbeta。在慢性炎症性疾病中触发促炎细胞因子产生的一个重要机制是刺激的T细胞与单核巨噬细胞之间的直接细胞接触。这一机制在系统水平上被“阴性”的急性时相蛋白载脂蛋白A-I(apo A-I)阻断。细胞因子、细胞因子抑制物和急性期蛋白的表达水平受激素控制。雌激素和雄激素一样能抑制单核巨噬细胞产生IL-1β和TNF-α。然而，雄激素通过肝脏拮抗雌激素对载脂蛋白A-I合成的刺激作用。其他研究表明，雌二醇对Th1细胞因子(如IFN-γ、IL-2)的抑制作用更强，而睾酮对Th2细胞因子(如IL-4)的抑制作用更强。细胞因子也控制着下丘脑-垂体腺-肾上腺的轴以及性激素。研究之间的差异表明，这些机制在生理和病理生理条件下是不同的。
The cytokine network is a homeostatic system that has to be perceived in an analogous fashion to the acid/base equilibrium. The level of any cytokine in biological fluids can be interpreted correctly only by taking into account the levels of other synergistic cytokines, of their respective inhibitors. and of each cytokine receptor. Due to their potent activities in many different processes (including cell growth and differentiation, development, and repair processes leading to the restoration of homeostasis), the cytokine activities have to be tightly controlled by natural inhibitory mechanisms. Since one of the main functions of cytokines is to mediate interactions between the immune and inflammatory system, it is thought that chronic immuno-inflammatory diseases might be caused in part by the uncontrolled production of cytokines. Depending on the stage of inflammation or the biological effect determined, the same cytokine might be pro- or anti-inflammatory. This applies, for instance, to IL-4, IL-10, and TGFbeta. An important mechanism that triggers the production of pro- inflammatory cytokines In chronic inflammatory diseases Is the direct cellular contact between stimulated T cells and monocyte-macrophages. This mechanism is blocked at the systemic level by the "negative" acute-phase protein apolipoprotein A-I (apo A-I). The levels of expression of cytokines and cytokine inhibitors and acute-phase proteins are ruled by hormones. Estrogens as well as androgens inhibit the production of IL-1beta and TNF-alpha on monocyte-macrophages. However, androgens antagonize estrogen stimulatory effects on apo A-I synthesis by the liver. Other studies suggest that estradiol is more inhibitory to Thl cytokines (e.g., IFNgamma, IL-2), while testosterone is Inhibitory to Th2 cytokines (e.g., IL-4). Cytokines also control the axis of the hypothalamic-hypophyseal-adrenal glands as well as the sexual hormones. The discrepancy between studies would suggest that the mechanisms are different In physiological and pathophysiological conditions.