New research shows that ovaries change after a woman cannot have children. They stop making babies and start working with the immune system.

新研究顯示，女性在無法生育後卵巢會發生變化。它們停止產生胚胎，並開始與免疫系統協作。

Scientists thought ovaries did nothing after menopause. But Francesca Duncan studied women and mice. She found that ovaries change over many years.

科學家原以為卵巢在更年期後便不再有功能。但 Francesca Duncan 研究了女性與小鼠，發現卵巢在多年時間裡會持續發生變化。

In old mice, the ovaries stopped making eggs. Instead, they started making more immune cells. These cells can cause inflammation in the body.

在年老的小鼠中，卵巢停止產生卵子。相反地，它們開始產生更多免疫細胞，而這些細胞可能會導致身體發炎。

Diana Laird says mice and humans are similar. She thinks this change happens in women too. This might cause health problems like joint pain in older women.

Diana Laird 表示小鼠與人類非常相似。她認為這種變化也會發生在女性身上，這可能會導致年長女性出現如關節疼痛等健康問題。

The study shows that old ovaries can cause inflammation. Scientists need to study this more.

研究顯示，年老的卵巢可能會導致發炎。科學家需要對此進行更多研究。

Recent research suggests that after women stop being fertile, their ovaries may change from reproductive organs into sites of immune activity.

近期研究指出，女性在停止生育後，其卵巢可能會從生殖器官轉變為免疫活動的場所。

For a long time, scientists believed that ovaries remained inactive after menopause. However, Francesca Duncan from Northwestern University analyzed protein levels in women aged 50 to 75 and found that molecular patterns change over several decades. To study this, researchers used a mouse model to compare three different ages: young, old, and post-reproductive.

長期以來，科學家認為卵巢在更年期後便不再具有活性。然而，西北大學的 Francesca Duncan 分析了 50 至 75 歲女性的蛋白質水平，發現分子模式在數十年間會發生改變。為了研究這一點，研究人員使用小鼠模型來比較三個不同的年齡層：年輕、年老以及生育期後。

As expected, the researchers found a decrease in genes that produce estradiol and a loss of follicles. Furthermore, the data showed an increase in genes related to inflammation, specifically a rise in T cells and macrophages within the ovarian tissue. This suggests that the ovary shifts its identity from reproduction to immunity. Consequently, this process may contribute to 'inflammaging,' which is a state of chronic, low-grade inflammation throughout the body.

正如預期，研究人員發現產生雌二醇的基因減少且卵泡流失。此外，數據顯示與發炎相關的基因增加，特別是卵巢組織內的 T 細胞和巨噬細胞增加。這顯示卵巢的身分從生殖轉向了免疫。因此，這一過程可能會導致「炎齡化」（inflammaging），即一種全身性的慢性低度發炎狀態。

Although the study used mice, Diana Laird from the University of California, San Francisco, emphasized that the biological similarities between species make these findings relevant to humans. She asserted that while having a reservoir of immune cells might have been an evolutionary advantage in the past, it may now make post-menopausal women more likely to develop autoimmune diseases, such as rheumatoid arthritis.

儘管該研究使用小鼠，但加州大學舊金山分校的 Diana Laird 強調，物種之間的生物學相似性使得這些發現對人類具有參考價值。她斷言，雖然擁有免疫細胞儲備在過去可能是進化上的優勢，但現在可能會使更年期後的女性更容易患上自體免疫疾病，例如類風濕性關節炎。

The study indicates that ovaries after the reproductive stage may actively cause systemic inflammation, which means more detailed molecular research is needed.

研究指出，生育期後的卵巢可能會主動引起全身性發炎，這意味著需要更詳細的分子研究。

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。