Cutolo M, Wilder R L
Department of Internal Medicine, University of Genova, Italy.
Rheum Dis Clin North Am. 2000 Nov;26(4):825-39. doi: 10.1016/s0889-857x(05)70171-x.
It is now documented that androgens and estrogens modulate susceptibility and progression to autoimmune rheumatic diseases. At any concentration, androgens seem to be primarily suppressive on cellular and humoral immunity, whereas at physiologic concentrations, estrogens seem to enhance humoral immunity. Further research should focus on the different and frequently opposite effects exerted by physiologic and pharmacologic doses of estrogens (dose-related effects). In addition to the influence of endogenous estrogen fluctuations (i.e., during pregnancy, postpartum, menstrual periods, menopause), estrogen replacement therapy, and the use of oral contraceptives, the susceptibility to autoimmunity might be increased by the environmental estrogens (xenobiotics). Further studies must be directed to the inflammatory mediators (i.e., cytokines) that seem to alter the peripheral metabolism of sex hormones and complicate the effects of sex hormones on susceptibility to autoimmunity. Finally, genetic factors might further interfere with the roles of androgens and estrogens in selected individuals.
现已证明，雄激素和雌激素可调节自身免疫性风湿疾病的易感性及病情进展。在任何浓度下，雄激素似乎主要抑制细胞免疫和体液免疫，而在生理浓度下，雌激素似乎增强体液免疫。进一步的研究应聚焦于生理剂量和药理剂量雌激素所产生的不同且往往相反的效应（剂量相关效应）。除了内源性雌激素波动（即孕期、产后、经期、更年期期间）、雌激素替代疗法及口服避孕药的影响外，环境雌激素（外源性生物活性物质）可能会增加自身免疫易感性。必须进一步研究炎症介质（即细胞因子），它们似乎会改变性激素的外周代谢，并使性激素对自身免疫易感性的影响复杂化。最后，遗传因素可能会在特定个体中进一步干扰雄激素和雌激素的作用。
