Effects of inactivated HIV-1 particles on expressions of CD25, CD71, and HLA-DR on human CD4+T cells

HUANG Xiuyan; ZENG Yaoying; WANG Hui

Abstract：Objective To explore the pathological mechanisms of immune overactivation in HIV disease by investigating the effects of AT-2-incetivated HIV-1 particles on expression of CD25, CD71 and HLA-DR on CD4+T cells from human peripheral blood mononuclear cells (PBMCs). Methods HIV-1ⅢB particles were inactivated by AT-2 and the concentration of p24 antigen was quanti-tated by p24 ELISA, then the AT-2-inactivated HIV-1ⅢB particles were added to human PBMCs culture system in serial concentrations to stimulate cells, with PHA group as the positive control. After 24 h, the percentage of CD25 expression on CD4+ T cells from PBMCswas detected by immuno-fluorescence staining plus flow cytometry; after 48 h, the percentage of CD71 and HLA-DR expression on CD4+T cells from PBMCs were detected by immuno-fluorescence staining plus flow cytometry. Results The concentration of p24 anti-gen in the prepared AT-2-inactivated specimen was 80 ng/mL, which was then diluted to 50 ng/mL. 24 h later, the percentage of CD25expression on CD4+T cells from control group was (9.46±2.12) %, whereas the CD25 expression were (79.45±3.72) %, ( 14.89±2.53)% , (19.04±2.41)% and (23.50±2.21)% in PHA group, HIV-11/500 group, HIV-1 /50 group, and HIV-11/5group, respectively. 48 h later, the percentage of CD71 expression on CD4+T cells from control group was (3.39±1.40)%, whereas the CD71 expression were (75.52±5.14)%, (11.70±2.34)%, (18.45±3.19)% and (22.59±2.96)% in PHA group, HIV-1 1/500 group, HIV-11/50 group, and HIV-11/5 group, respectively; the percentage of HLA-DR expression on CD4+ T cells from control group was (8.11±2.13)%, whereas the HLA-DR expression were (66.48±6.81 )%, ( 14.52±1.68)%, ( 19.94±2.38) %, and (23.74±2.30) % in PHA group, HIV-1 1/500 group,HIV-11/50 group, and HIV-11/5 group, respectively. Conclusion AT-2-inactivated HIV-1ⅢB particles could strikingly activate CD4+ T ceils from PBMCs, and may cause CD4+T cells proliferation, which can offer HIV-1 more "fuel cells".