المؤلفون: Wang, Fuyan, Qualls, Anita Ellen, Marques-Fernandez, Laia, Colucci, Francesco

المساهمون: Wellcome Trust, National Natural Science Foundation of China

المصدر: Cellular & Molecular Immunology ; volume 18, issue 9, page 2101-2113 ; ISSN 1672-7681 2042-0226

مصطلحات موضوعية: Infectious Diseases, Immunology, Immunology and Allergy

الوصف: Tissues are the new frontier of discoveries in immunology. Cells of the immune system are an integral part of tissue physiology and immunity. Determining how immune cells inhabit, housekeep, and defend gut, lung, brain, liver, uterus, and other organs helps revealing the intimate details of tissue physiology and may offer new therapeutic targets to treat pathologies. The uterine microenvironment modulates the development and function of innate lymphoid cells [ILC, largely represented by natural killer (NK) cells], macrophages, T cells, and dendritic cells. These immune cells, in turn, contribute to tissue homeostasis. Regulated by ovarian hormones, the human uterine mucosa (endometrium) undergoes ~400 monthly cycles of breakdown and regeneration from menarche to menopause, with its fibroblasts, glands, blood vessels, and immune cells remodeling the tissue into the transient decidua. Even more transformative changes occur upon blastocyst implantation. Before the placenta is formed, the endometrial glands feed the embryo by histiotrophic nutrition while the uterine spiral arteries are stripped of their endothelial layer and smooth muscle actin. This arterial remodeling is carried out by invading fetal trophoblast and maternal immune cells, chiefly uterine NK (uNK) cells, which also assist fetal growth. The transformed arteries no longer respond to maternal stimuli and meet the increasing demands of the growing fetus. This review focuses on how the everchanging uterine microenvironment affects uNK cells and how uNK cells regulate homeostasis of the decidua, placenta development, and fetal growth. Determining these pathways will help understand the causes of major pregnancy complications.

الإتاحة: https://doi.org/10.1038/s41423-021-00739-zTest
https://www.nature.com/articles/s41423-021-00739-z.pdfTest
https://www.nature.com/articles/s41423-021-00739-zTest

المؤلفون: Deng, Haiyan, Zhang, Pingping, Gao, Xianxian, Chen, Weiyi, Li, Jianing, Wang, Fuyan, Gu, Yiyue, Hou, Xin

المساهمون: Natural Science Foundation of Zhejiang Province, Natural Science Foundation of Ningbo Municipality, Ningbo Municipal Natural Science Foundation, National Natural Science Foundation of China

المصدر: International Immunopharmacology ; volume 114, page 109598 ; ISSN 1567-5769

مصطلحات موضوعية: Pharmacology, Immunology, Immunology and Allergy

الإتاحة: https://doi.org/10.1016/j.intimp.2022.109598Test
https://api.elsevier.com/content/article/PII:S1567576922010839?httpAccept=text/xmlTest
https://api.elsevier.com/content/article/PII:S1567576922010839?httpAccept=text/plainTest

المؤلفون: Peng, Bo, Peng, Na, Zhang, Yanan, Zhang, Fenghua, Li, Xuguang, Chang, Haiyan, Fang, Fang, Wang, Fuyan, Lu, Fangguo, Chen, Ze

المصدر: Frontiers in Immunology ; volume 8 ; ISSN 1664-3224

مصطلحات موضوعية: Immunology, Immunology and Allergy

الإتاحة: https://doi.org/10.3389/fimmu.2017.01070Test

المؤلفون: Lu, Xiaofang, Wang, Yong, Ma, Ying, Huang, Dong, Lu, Yuying, Liu, Xiang, Zhou, Ruijia, Yu, Ping, Zhang, Lei, Chen, Jianlin, Lu, Rong, Wang, Fuyan

المساهمون: Natural Science Foundation of Hunan Province

المصدر: Immunology Letters ; volume 242, page 8-16 ; ISSN 0165-2478

مصطلحات موضوعية: Immunology, Immunology and Allergy

الإتاحة: https://doi.org/10.1016/j.imlet.2021.12.003Test
https://api.elsevier.com/content/article/PII:S0165247821001838?httpAccept=text/xmlTest
https://api.elsevier.com/content/article/PII:S0165247821001838?httpAccept=text/plainTest

المؤلفون: Liu, Siqi, Liu, Qi, Xie, Huiyuan, Li, Minmin, Wang, Fuyan, Shen, Jijia, Liu, Miao, Ren, Cuiping, Hou, Xin

المساهمون: National Natural Science Foundation of China

المصدر: Journal of Reproductive Immunology ; volume 145, page 103312 ; ISSN 0165-0378

مصطلحات موضوعية: Obstetrics and Gynecology, Reproductive Medicine, Immunology, Immunology and Allergy

الإتاحة: https://doi.org/10.1016/j.jri.2021.103312Test
https://api.elsevier.com/content/article/PII:S0165037821000425?httpAccept=text/xmlTest
https://api.elsevier.com/content/article/PII:S0165037821000425?httpAccept=text/plainTest

المؤلفون: Wu, Junhua, Wu, Danyang, Zhang, Longyao, Lin, Chuxuan, Liao, Jiahao, Xie, Ruyin, Li, Zhulin, Wu, Siyang, Liu, Aimin, Hu, Weining, Xi, Yang, Bu, Shizhong, Wang, Fuyan

المساهمون: Natural Science Foundation of Zhejiang Province, National Natural Science Foundation of China, Ningbo Science and Technology Innovation Team Program, Natural Science Foundation of Ningbo Municipality, Natural Science Foundation of Ningbo

المصدر: Journal of Leukocyte Biology ; volume 107, issue 4, page 589-596 ; ISSN 1938-3673 0741-5400

مصطلحات موضوعية: Cell Biology, Immunology, Immunology and Allergy

الوصف: High-fat diet (HFD) induced hepatic endoplasmic reticulum (ER) stress drives insulin resistance (IR) and steatosis. NK cells in adipose tissue play an important role in the pathogenesis of IR in obesity. Whether NK cells in the liver can induce hepatic ER stress and thus promote IR in obesity is still unknown. We demonstrate that HFD-fed mice display elevated production of proinflammatory cytokine osteopontin (OPN) in hepatic NK cells, especially in CD49a+DX5– tissue-resident NK (trNK) cells. Obesity-induced ER stress, IR, and steatosis in the liver are ameliorated by ablating NK cells with neutralizing antibody in HFD-fed mice. OPN treatment enhances the expression of ER stress markers, including p-PERK, p-eIF2, ATF4, and CHOP in both murine liver tissues and HL-7702, a human liver cell line. Pretreatment of HL-7702 cells with OPN promotes hyperactivation of JNK and subsequent decrease of tyrosine phosphorylation of insulin receptor substrate-1 (IRS-1), resulting in impaired insulin signaling, which can be reversed by inhibiting ER stress. Collectively, we demonstrate that hepatic NK cells induce obesity-induced hepatic ER stress, and IR through OPN production.

الإتاحة: https://doi.org/10.1002/jlb.3ma1119-173rTest
https://academic.oup.com/jleukbio/article-pdf/107/4/589/48795867/jlb10522.pdfTest