Recent research indicates that ovaries may transition from reproductive organs to immune-active sites following the cessation of fertility.

最近的研究指出，卵巢在失去生育能力後，可能會從生殖器官轉變為免疫活躍部位。

The prevailing scientific consensus previously posited that post-menopausal ovaries remained biologically inert. However, preliminary analysis of protein compositions in women aged 50 to 75, conducted by Francesca Duncan of Northwestern University, suggests a dynamic shift in molecular signatures over several decades. To examine this phenomenon, a murine model was employed, comparing subjects across three developmental stages: young (2 months), reproductively old (18 months), and post-reproductive (24 months).

先前科學界的普遍共識認為，停經後的卵巢在生物學上保持不活躍狀態。然而，西北大學的 Francesca Duncan 對 50 至 75 歲女性的蛋白質組成進行初步分析，結果顯示分子標誌在數十年間有動態偏移。為了探討此現象，研究採用了小鼠模型，比較三個發育階段的對象：年輕（2 個月）、生殖期年老（18 個月）以及生育期後（24 個月）。

While the downregulation of estradiol-producing genes and the depletion of follicles were observed as expected, the data revealed a concomitant increase in the expression of genes associated with inflammatory responses. Specifically, there was a documented proliferation of macrophages and T cells within the ovarian tissue. This transition suggests a shift from a reproductive identity to an immunological one, potentially contributing to 'inflammaging'—a state of chronic, low-grade systemic inflammation—via the secretion of inflammatory signaling molecules.

雖然如預期地觀察到產生雌二醇的基因下調及卵泡耗盡，但數據揭示與發炎反應相關的基因表達隨之增加。具體而言，卵巢組織內的巨噬細胞與 T 細胞記錄到增殖現象。這種轉變顯示其從生殖身份轉向免疫身份，可能透過分泌發炎信號分子，促成「炎性衰老」——即一種慢性、低等級的全身性發炎狀態。

Although the primary data is derived from murine subjects, Diana Laird of the University of California, San Francisco, posits that the biological parallels between the species—specifically the cessation of cycling upon reaching a critical oocyte threshold and shared fibrotic changes—render these findings applicable to humans. It is hypothesized that while the development of an immune cell reservoir may have provided evolutionary advantages in previous epochs, it may now predispose individuals to autoimmune pathologies, such as rheumatoid arthritis, in the post-menopausal period.

儘管主要數據源自小鼠對象，但加州大學舊金山分校的 Diana Laird 主張，物種間的生物學平行之處——特別是在達到關鍵卵母細胞閾值後停止週期以及共同的纖維化變化——使得這些發現適用於人類。據假設，雖然發展免疫細胞儲備在過往時代可能提供演化優勢，但現在可能使個體在停經後易於患上自身免疫疾病，例如類風濕性關節炎。

The study suggests that post-reproductive ovaries may actively contribute to systemic inflammation, necessitating further functional molecular research.

研究顯示，生育期後的卵巢可能會主動促成全身性發炎，因此有必要進行進一步的功能分子研究。