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。