Coulam C B, Stern J J
Center for Reproduction and Transplantation Immunology, Methodist Hospital of Indiana, Inc., Indianapolis 46202.
Am J Reprod Immunol. 1991 May;25(4):169-74. doi: 10.1111/j.1600-0897.1991.tb01089.x.
Ovarian failure is the result of depletion of ovarian follicles. Naturally occurring ovarian failure usually takes place around 50 years of age in the human. Premature ovarian failure occurs in 1% of women and is the result of acceleration of rate of ovarian follicular depletion in the majority of cases. Cytokines are involved in the mechanisms of ovarian follicular atresia, whether it occurs at a normal or accelerated rate. It is the balance between the actions of TGF alpha and TGF beta upon the granulosa cell that determines the fate of a nonluteinized follicle and between LH and INF gamma that determines destiny of a luteinized follicle. When granulosa cells express MHC antigens in response to IFN gamma or genetic stimulus, an autoimmune reaction ensures resulting in follicular atresia. If the immune processes proceed continuously rather than cyclically, premature ovarian failure occurs. Thus, not only do the immunologic and endocrinologic systems need to communicate to allow normal ovarian function, evidence exists to support the concept that they interact in the pathophysiology of ovarian failure.
卵巢功能衰竭是卵巢卵泡耗竭的结果。在人类中，自然发生的卵巢功能衰竭通常发生在50岁左右。1%的女性会发生卵巢早衰，在大多数情况下，这是卵巢卵泡耗竭速度加快的结果。细胞因子参与卵巢卵泡闭锁的机制，无论其发生速度是正常还是加快。正是转化生长因子α（TGFα）和转化生长因子β（TGFβ）对颗粒细胞作用之间的平衡决定了未黄体化卵泡的命运，而促黄体生成素（LH）和干扰素γ（INFγ）之间的平衡决定了黄体化卵泡的命运。当颗粒细胞响应干扰素γ或基因刺激表达主要组织相容性复合体（MHC）抗原时，会引发自身免疫反应，导致卵泡闭锁。如果免疫过程持续进行而非周期性发生，就会出现卵巢早衰。因此，免疫和内分泌系统不仅需要相互沟通以实现正常的卵巢功能，而且有证据支持它们在卵巢功能衰竭的病理生理学中相互作用这一概念。
