دورية أكاديمية

Exosomes from dendritic cells with Mettl3 gene knockdown prevent immune rejection in a mouse cardiac allograft model.

التفاصيل البيبلوغرافية
العنوان: Exosomes from dendritic cells with Mettl3 gene knockdown prevent immune rejection in a mouse cardiac allograft model.
المؤلفون: Wu H; Department of Cardiovascular Surgery, Renmin Hospital of Wuhan University; Hubei Cardiovascular Medicine Clinical Research Center & Hubei Key Laboratory of Cardiology, 238# Jiefang Road, Wuchang District, Hubei Province, Wuhan, China., Xu Z; Department of Critical Care Medicine, Jin Yin-tan Hospital, 1# Yin-Tan Road, Dongxihu District, Hubei Province, Wuhan, China., Wang Z; Department of Cardiovascular Surgery, Renmin Hospital of Wuhan University; Hubei Cardiovascular Medicine Clinical Research Center & Hubei Key Laboratory of Cardiology, 238# Jiefang Road, Wuchang District, Hubei Province, Wuhan, China. wangzwei60@163.com., Ren Z; Department of Cardiovascular Surgery, Renmin Hospital of Wuhan University; Hubei Cardiovascular Medicine Clinical Research Center & Hubei Key Laboratory of Cardiology, 238# Jiefang Road, Wuchang District, Hubei Province, Wuhan, China., Li L; Department of Cardiovascular Surgery, Renmin Hospital of Wuhan University; Hubei Cardiovascular Medicine Clinical Research Center & Hubei Key Laboratory of Cardiology, 238# Jiefang Road, Wuchang District, Hubei Province, Wuhan, China., Ruan Y; Department of Cardiovascular Surgery, Renmin Hospital of Wuhan University; Hubei Cardiovascular Medicine Clinical Research Center & Hubei Key Laboratory of Cardiology, 238# Jiefang Road, Wuchang District, Hubei Province, Wuhan, China.
المصدر: Immunogenetics [Immunogenetics] 2020 Oct; Vol. 72 (8), pp. 423-430. Date of Electronic Publication: 2020 Oct 03.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Springer Verlag Country of Publication: United States NLM ID: 0420404 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1432-1211 (Electronic) Linking ISSN: 00937711 NLM ISO Abbreviation: Immunogenetics Subsets: MEDLINE
أسماء مطبوعة: Original Publication: New York, NY : Springer Verlag,
مواضيع طبية MeSH: Dendritic Cells/*cytology , Exosomes/*metabolism , Graft Rejection/*prevention & control , Heart Transplantation/*adverse effects , Immune Tolerance/*immunology , Methyltransferases/*antagonists & inhibitors , T-Lymphocytes, Regulatory/*immunology, Allografts ; Animals ; Gene Knockdown Techniques ; Graft Rejection/etiology ; Graft Rejection/metabolism ; Graft Rejection/pathology ; Male ; Methyltransferases/genetics ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL
مستخلص: We have previously demonstrated that Mettl3-silencing dendritic cells (DCs) exhibited immature properties and prolonged allograft survival in a murine heart transplantation model. Exosomes derived from donor DCs (Dex) are involved in the immune rejection of organ transplantation, and blocking Dex transfer may suppress immune rejection. Herein, this study aimed to investigate whether Mettl3 knockdown inhibits the secretion and activity of donor Dex, thereby inhibiting donor Dex-mediated immune rejection. The imDex, mDex, shCtrl-mDex, and shMettl3-mDex were obtained from the culture supernatant of DCs (immature DCs, mature DCs, shCtrl-infected mature DCs, shMettl3-infected mature DCs) derived from donor BALB/c mouse bone marrow and then co-cultured with splenic T cell lymphocyte suspension from recipient C57BL/6 mice in vitro or injected into recipient C57BL/6 mice before the cardiac transplantation. Donor shMettl3-mDex expressed lower concentration of exosomes and lower expression of Mettl3, Dex markers (ICAM-1, MHC-I, MHC-II), as well as lower ability to activate T cell immune response than shCtrl-mDex. Administration of donor shMettl3-mDex attenuated immune rejection after mouse heart transplantation and prolonged the allograft survival. In summary, Mettl3 knockdown inhibits the immune rejection of Dex in a mouse cardiac allograft model.
فهرسة مساهمة: Keywords: Dendritic cell; Heart transplantation; Immune response; Mettl3
المشرفين على المادة: EC 2.1.1.- (Methyltransferases)
EC 2.1.1.- (Mettl3 protein, mouse)
تواريخ الأحداث: Date Created: 20201003 Date Completed: 20210201 Latest Revision: 20210201
رمز التحديث: 20240829
DOI: 10.1007/s00251-020-01180-8
PMID: 33009922
قاعدة البيانات: MEDLINE
الوصف
تدمد:1432-1211
DOI:10.1007/s00251-020-01180-8