- Author:
Bing-Liang LIN
1
;
Dong-Ying XIE
;
Jun-Qiang XIE
;
Xiao-Hong ZHANG
;
Yong-Yu MEI
;
Zhi-Liang GAO
Author Information
- Publication Type:Journal Article
- MeSH: Adolescent; Adult; Carrier State; blood; immunology; virology; Case-Control Studies; Hepatitis B; blood; immunology; Hepatitis B Antigens; blood; Hepatitis B virus; immunology; Humans; Interferon-gamma; blood; Interleukin-12; blood; immunology; Leukocytes, Mononuclear; immunology; T-Lymphocytes; immunology; Young Adult
- From: Chinese Journal of Hepatology 2011;19(3):186-190
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effect of HBV antigens and pathological mechanism of chronic HBV infection by analyzing the cellular immune function of peripheral blood mononuclear cells (PBMCs) from HBsAg carriers.
METHODSPBMCs were prepared from individuals with chronic asymptomatic HBV infection and cultured in the presence of different antigens and/ or cytokines. The levels of cytokines in culture supernatants were detected by ELISA method. The phenotype of the cells was detected by FACS.
RESULTSThe levels of IFN y secreted by PBMCs from HBsAg carriers were (48.3+/-19.8) pg/ml, significantly lower than that from healthy controls (t = 3.023, P less than 0.05); The IFN y produced by PBMCs from HBeAg positive patients due to HBsAg and HBcAg stimulation were (50.4+/-51.6) pg/ml and (63.2+/-36.9) pg/ml, significantly lower than that of HBeAg negative patients (t = 2.468 and 3.184, P less than 0.05, respectively). The IL-12p70 secreted by PBMCs from HBeAg positive patients was also significantly lower than that of HBeAg negative patients (P less than 0.05); Exogenous IL-12 promoted significantly PBMCs to secrete IFN y (P less than 0.01) and IL-12 combined with HBV antigens activated CD8+CD45RA+CCR7+ and CD8+CD45RA-CD62L+ cells. IL-12 secreted by PBMCs decreased in HBeAg positive patients, which may be the crucial reason of viral persistence in chronic HBV carriers. Exogenous IL-12 combined with specific HBV antigen could promote the central memory CD8+ T cells to produce IFN y.