Soluble IgM links apoptosis to complement activation in early alcoholic liver disease in mice
详细信息 查看全文
- 作者：Rebecca L. Smathersa ; 1 ; Dian J. Chianga ; b ; 1 ; 2 ; Megan R. McMullena ; Ariel E. Feldsteind ; Sanjoy Roychowdhurya ; Laura E. Nagya ; b ; c ; nagyL3@ccf.org" class="auth_mail" title="E-mail the corresponding author
- 关键词：ALT ; alanine aminotransferase activity ; ASH ; alcoholic hepatitis ; C1INH ; C1 inhibitor (Cinryze) ; C3 ; third component of the complement system ; C3b ; C3b-iC3b/C3c ; C5 ; fifth component of the complement system ; C3aR ; C3a receptor ; C5aR ; C5a receptor ; CR ; complement receptor ; CYP2E1 ; cytochrome P450 2E1 ; DAF ; decay accelerating factor ; FBS ; fetal bovine serum ; IL-6 ; interleukin 6 ; IFNγ ; interferon γ ; LPS ; lipopolysaccharide ; OCT ; optimal cutting temperature ; PBS ; phosphate buffered saline ; ROS ; reac
- 刊名：Molecular Immunology
- 出版年：2016
- 出版时间：April 2016
- 年：2016
- 卷：72
- 期：Complete
- 页码：9-18
- 全文大小：4901 K
文摘
- •
The progression of ethanol-induced liver injury was studied in a mouse model.
- •
IgM co-localizes with C1q in the liver in response to ethanol feeding; accumulation of IgM and C3b at early stages of ethanol feeding is dependent on apoptosis.
- •
sIgM−/− mice are protected from early stages of ethanol-induced liver injury.
- •
C1INH, an inhibitor of C1 activity, protected from ethanol-induced liver injury