Recent insight into autophagy and immunity at the maternal-fetal interface. (February 2023)

• Record Type: Journal Article
• Authors: Chen, Yuanyao; Xiao, Lin; Xu, Jia; Wang, Jingming; Yu, Zhiquan; Zhao, Kai; Zhang, Huiping; Cheng, Shibin; Sharma, Surendra; Liao, Aihua; Liu, Chunyan
• Is Part Of: Journal of reproductive immunology. Volume 155(2023)
• Publication Date: 2023-02
• Subjects: Autophagy -- maternal-fetal interface -- innate immunity -- adaptive immunity -- immune tolerance molecules; Reproduction -- Immunological aspects -- Periodicals; Immunology -- Periodicals; Allergy and Immunology -- Periodicals; Reproduction -- Periodicals; Reproduction -- Immunologie -- Périodiques; Immunologie -- Périodiques; Immunology; Reproduction -- Immunological aspects; Periodicals; Electronic journals; Electronic journals; 615.766
• DOI: 10.1016/j.jri.2022.103781
• Languages: English
• ISSNs: 0165-0378

Abstract

Abstract: Autophagy is a lysosomal degradation pathway that supports metabolic adaptation and energy cycling. It is essential for cell homeostasis, differentiation, development, and survival. Recent studies have shown that autophagy could influence immune responses by regulating immune cell functions. Reciprocally, immune cells strongly influence autophagy. Immune cells at the maternal-fetal interface are thought to play essential roles in pregnancy. Here, we review the induction of autophagy at the maternal-fetal interface and its role in decidualization and placental development. Additionally, we emphasize the role of autophagy in the immune microenvironment at the maternal-fetal interface, including innate immunity, adaptive immunity, and immune tolerance molecules. It also suggests new research directions and prospects. Highlights: Autophagy can be induced by microenvironmental factors at the maternal-fetal interface. Autophagy involves endometrial decidualization and placental development. Autophagy affects immune response by regulating innate and adaptive immune cell functions at the maternal-fetal interface.