Stress hormones, proinflammatory and antiinflammatory cytokines, and autoimmunity
Stress hormones, proinflammatory and antiinflammatory cytokines, and autoimmunity
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DOI：
10.1111/j.1749-6632.2002.tb04229.x
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发表时间：
2002-01-01
期刊：
影响因子：
--
通讯作者：
Chrousos, GP
中科院分区：
文献类型：
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作者：
Elenkov, IJ;Chrousos, GP
最近的证据表明，糖皮质激素和儿茶酚胺作为主要的应激激素，抑制促炎细胞因子的产生，如白介素12、肿瘤坏死因子α和干扰素γ，而它们刺激抗炎细胞因子的产生，如白介素10、白介素4和转化生长因子β。因此，从系统上讲，过度的免疫反应通过激活应激系统，刺激一种重要的负反馈机制，保护机体免受促炎细胞因子和具有组织损伤潜力的激活巨噬细胞产生的其他产物的影响。相反，在某些局部反应和特定条件下，应激激素实际上可能通过诱导肿瘤坏死因子-α、IL-1和IL-8以及抑制转化生长因子-β的产生来增强局部免疫反应。因此，与应激系统活动显著变化相关的条件，如急性或慢性应激、停止慢性应激、剧烈运动、妊娠和产后，通过调节全身或局部促炎/抗炎细胞因子平衡，可能抑制或增强自身免疫性疾病的活动和/或进展。
Recent evidence indicates that glucocorticolds and catecholamines, the major stress hormones, inhibit the production of proinflammatory cytokines, such as interleukin (IL)-12, tumor necrosis factor (TNF)-alpha, and interferon (IFN)-gamma, whereas they stimulate the production of antiinflammatory cytokines, such as IL-10, IL-4, and transforming growth factor (TGF)-beta. Thus, systemically, an excessive immune response, through activation of the stress system, stimulates an important negative feedback mechanism, which protects the organism from an "overshoot" of proinflammatory cytokines and other products of activated macrophages with tissue-damaging potential. Conversely, in certain local responses and under certain conditions, stress hormones actually may boost regional immune responses, through induction of TNF-alpha, IL-1, and IL-8, and by inhibiting TGF-beta production. Therefore, conditions that are associated with significant changes in stress system activity, such as acute or chronic stress, cessation of chronic stress, severe exercise, and pregnancy and the postpartum period, through modulation of the systemic or local pro/antiinflammatory cytokine balance, may suppress or potentiate autoimmune diseases activity and/or progression.