Effects of inactivated HIV-1 particles on human CD4~+T cell activation and Th1/Th2 cytokine secretion in whole blood / 中国病理生理杂志
Chinese Journal of Pathophysiology
; (12)2000.
Article
em Zh
| WPRIM
| ID: wpr-531406
Biblioteca responsável:
WPRO
ABSTRACT
AIM:To investigate the effects of AT-2-inactivated HIV-1 particles on human CD4+T cell activation and cytokine secretion in whole blood (WB) in vitro. METHODS: HIV-1ⅢB particles were inactivated by AT-2 chemical and the concentration of p24 antigen was determined by p24 ELISA. AT-2-inactivated HIV-1ⅢB particles were added to human WB culture system in serial concentrations to stimulate the cells. PHA was used as positive control. After 24 h, all the cultural supernatants were harvested and the concentrations of Th1 (IL-2, IFN-? and TNF-?) and Th2 (IL-4, IL-6 and IL-10) cytokines released to the supernatants were detected by cytometric bead array (CBA). The percentage of CD69 expression on CD4+T cells from WB was detected by immuno-fluorescence staining plus flow cytometry. RESULTS: The concentration of p24 antigen in the AT-2-inactivated specimen was 85.5 ?g/L. 24 h later, the percentage of CD69 expression on CD4+T cells from control group was (1.62?0.63) %, whereas it was (38.82?6.00)%, (3.83?1.07)%, (5.94?0.85)% and (9.30?1.22)% in PHA group, HIV-1 (1/500) group, HIV-1 (1/50) group and HIV-1 (1/5) group, respectively. Cytokines secreted by WB in control group were mainly TNF-? and IL-6. However, all the six cytokines tested were strikingly increased in PHA group, as well as in HIV-1ⅢB groups. CONCLUSION: AT-2-inactivated HIV-1ⅢB particles activate CD4+T cells from WB, and up-regulate both Th1 and Th2 cytokine secretion in WB. Besides the effects of viral proteins, other mechanisms may be proposed that HIV-1 particles act as antigen presenting cell (APC) because many host-derived immune molecules are incorporated into HIV-1 envelop when it is released from infected cells by budding, and exert immune modulation.
Texto completo:
1
Base de dados:
WPRIM
Idioma:
Zh
Revista:
Chinese Journal of Pathophysiology
Ano de publicação:
2000
Tipo de documento:
Article