Prevention of primary biliary cirrhosis through immune tolerance reestablishment in a mouse model
10.3760/cma.j.issn.0254-5101.2011.05.009
- VernacularTitle:重建外周免疫耐受抑制原发性胆汁性肝硬化的实验研究
- Author:
Tingwang JIANG
;
Huaimin XIONG
;
Hongxing ZHANG
;
Yanping GONG
;
Anmei DENG
;
Renqian ZHONG
- Publication Type:Journal Article
- Keywords:
Primary biliary cirrhosis;
Model;
Immune tolerance
- From:
Chinese Journal of Microbiology and Immunology
2011;31(5):425-428
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate a new therapeutic pathway for primary biliary cirrhosis (PBC) by immune tolerance reestablishment in a PBC mouse model. Methods Spleenic cells from naive mice were incubated with M2 in the presence of ECDI and the ceils were injected into caudal vein of the mice which would be used for development of PBC model. Spleenic cells incubated with bovine serum albumin (BSA) were injected as controls. 16 weeks later, anti-mitoehondrial antibody (AMA) , alkaline phosphatase(AKP) and portal inflammation were assayed for evaluating the prevention effect. Results AMA positive rate in tolerance group was lower than that in BSA and PBC groups ( P = 0. 007, P = 0. 003 ). The difference between BSA and PBC was not significantly. Serum AKP levels in tolerance, BSA and PBC group were (80.5 ±9.8) U/L, (93.8 ±15.7) U/L and (92.5 ±17.7) U/L, separately. The level in tolerance group was lower than that in BSA and PBC groups (P =0.0095, P =0.029). The rates of portal areas with cell infiltration were 42. 67% ± 12. 30% , 57. 07% ± 11. 35% and 51. 53% ± 9. 96% , separately. The number of infiltrated portal tracts in tolerance group was less than that in PBC group (P = 0.039) and BSA group (P = 0. 0024). Conclusion PBC was prevented to some extent by reestablishing immune tolerance to M2 autoantigen. This provides clues for finding a better treatment proposal.