The study on the relationship between expression of B7-H1 on HBV transgenic mice and immune tolerance to HBV.
- Author:
Zhuo-Yi WANG
1
;
Jiang-Juan HE
;
Lei GENG
;
Lin ZHOU
;
Hai-Yang XIE
;
Jian WU
;
Shu-Sen ZHENG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Antigens, CD; biosynthesis; genetics; Cell Proliferation; Cytokines; biosynthesis; Dendritic Cells; immunology; metabolism; Flow Cytometry; Hepatitis B virus; genetics; immunology; Histocompatibility Antigens Class II; metabolism; Immune Tolerance; Liver; metabolism; Mice; Mice, Inbred BALB C; Mice, Inbred C57BL; Mice, Transgenic; RNA, Messenger; genetics; metabolism; Spleen; immunology; metabolism; T-Lymphocytes; immunology; metabolism
- From: Chinese Journal of Hepatology 2009;17(10):750-753
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate whether there is an association between the expression of B7-H1 in HBV transgenic mice and the immune tolerance to HBV.
METHODST cells stimulatory capacity of DC was analyzed using mixed lymphocyte reaction. Expression of MHC-II, CD80, CD86, B7-H1 on DC was detected by Flow Cytometry. IL-2, IFNgamma, IL-10 production of T cells were determined by using ELISA. B7-H1 mRNA and protein expression in liver tissue were detected by RT-PCR and Western blotting respectively.
RESULTSThe ability of DC cells from HBV transgenic mice to stimulate T cell proliferation was significantly impaired compared with DC cells from control mice (t = 16.674, 19.674, 21.712, P less than 0.01). Expression of MHC-II, CD80 on DC was markedly decreased in transgenic mice (t = 7.910, 6.413, P less than 0.05). Meanwhile, the expression of CD86 and B7-H1 on DC cells in HBV transgenic mice were not significantly different from that in control mice. The levels of IL-2, IFNgamma, IL-10 in supernatant of T cells was significantly lower compared with controls (t = 18.712, 18.712 and 11.683, P less than 0.05). There was no significant difference in B7-H1 expression at mRNA and protein levels in liver tissue compared with controls.
CONCLUSIONSFunctional defect of DC, partly due to decreased expression of MHC-II, CD80, but not related to B7-H1 expression, is the cause for immune tolerance to HBV in HBV transgenic mice.
