Abstract
The aims of this project were to investigate the effect of immune complexes on mononuclear phagocytes in the presence or absence of infection with the human immunodeficiency virus (HIV). Mono Mac 6 (MM6) cells and human monocyte-derived macrophages (MDM) were used to compare the effect of chemical stimulants, cytokines and immune complexes on surface antigen expression. The same experiments were performed using HIV-infected cells to determine the effect of HIV infection on these parameters. Some of the stimulants especially IL-6, IL-10, TNF-alpha and HIV increased CD80 expressions, the effect being greater in MDM than MM6 cells. This has implications for antigen presentation. Cytokines caused the differentiation of MM6 cells and significantly increased or decreased surface antigen expressions. The MM6 cells express surface antigens at lower levels then MDM this indicates that MM6 cells need to differentiate before expressing surface antigens. The high standard deviations obtained meant that no significant change in surface antigen expression was seen in all HIV non-infected and infected MDM incubated with various immune complexes and HIV-sera. Comparing whole blood incubated with KLH and rabbit anti-human IgG showed that both seemed to produce IL-10 and IL-6 early. Only rabbit complexes stimulated TNF-a release. MDM incubated with IL-6, IL-10, and TNF-alpha showed increased expression of CD16 and CD80 only at day 3. However, HIV proteins (CHO) incubated in whole blood caused a significantly release of IL-6 at 8 hours with no detection of IL-10 and TNF-alpha. MM6 infected with HIV-1 Ba-L for 5 days showed increased expression of CD16 and CD11c, but reduced expression of the other antigens examined. Significant levels of IL-10 were released at 8 and 12 hours with a slight increase in IL-6, and TNF-alpha. HIV protein-containing (CHO) immune complexes slightly increased IL-6 secretion at 8 hours at which point, IL-10 production was high. HIV- infected cells incubated with HlV-sera showed a lack of TNF-alpha release but IL-6 and IL-10 was detected at 12 and 8 hours respectively. The detection of high levels of IL-10 and the inhibition of TNF-alpha production may stimulate progression to full blown AIDS.