[
Clin Exp Immunol,
1983]
Lymphocyte blastogenic responses to O. volvulus antigen (Oncho Ag), SKSD, and the mitogen PHA were tested in three groups of persons: light to moderately infected persons (INF); previously exposed but uninfected persons (EXP) and normal controls (NC). The exposed group showed significant responsiveness to Oncho Ag (delta ct/min = 6,002 +/- 1,375), while the infected (delta ct/min = 943 +/- 418) and normal control (delta ct/min = 428 +/- 418) groups did not. The mean blastogenic response to SKSD were EXP, 8,644 +/- 5,249; NC 6,039 +/- 2,880; INF, 2,619 +/- 1,012. The reduced reactivity in the INF group to Oncho Ag showed a significant correlation with reactivity to SKSD (P less than 0.05). To elucidate the mechanism of hyporesponsiveness in the infected group rigorous adherent cell depletion, by adherence to plastic followed by a nylon wool column, was utilized. When 20% plastic adherent cells were added back to the T cells prepared in this fashion, the mean blastogenic response to SKSD was significantly augmented (P less than 0.01). In contrast, the responsiveness to Oncho Ag was not significantly altered. The addition of indomethacin (1 microgram/ml) or autologous plasma had no significant effect on reactivity to either SKSD or Oncho Ag. There were no significant differences in the mean reactivity of the three groups to PHA-M (delta ct/min EXP 78,514 +/- 12,564; INF 62,393 +/- 14,447; NC 61,423 +/- 4,465). These results suggest that O. volvulus infection is associated with decreased lymphocyte reactivity to both parasite related and unrelated antigens, and imply that the mechanism for the two types of hyporesponsiveness may be distinct. While a weakly adherent suppressor cell may account for non-specific hyporesponsiveness, the mechanism of parasite specific decreased reactivity remains unknown.
[
J Immunol,
1988]
Mechanisms involved in modulation of the immune response in persons with chronic Onchocerca volvulus infection are poorly understood. In this study in vitro reactivity of PBMC to O. volvulus antigen (Ovag), streptolysin O (SL-O) and the mitogen PHA was tested in 62 infected individuals (INF), 17 persons living in the endemic area with exposure to the infection, but with no detectable infection (END), and 7 healthy controls (CTRL) in Liberia, West Africa. Mean blastogenic responses to Ovag were minimal and did not differ between the groups. There was, however, heterogenous reactivity to Ovag in the INF and END. For example, individuals with a history of therapy, and half of those less than 17 yr old who were tested, showed high responses. No significant differences in the response to SL-O or PHA were detected between the groups. IL-2 production in response to Ovag was minimal in the majority of infected subjects. Exogenous IL-2 was found to cause a significant increase in mean responses to Ovag and SL-O in INF and END only. Similarly, Ovag did not stimulate IL-1 production in most INF, whereas stimulation with LPS led to significantly greater production of IL-1. Depletion of plastic and nylon wool adherent cells did not increase responses to parasite-related antigen in INF, END or CTRL; however, responses to SL-O were augmented in INF, an effect that was also observed in CTRL. Finally, depletion of CD8 or CD16 cells in INF by C lysis did not increase blastogenic responses. These results indicate that cell-mediated immunity to parasite-related Ag as reflected in lymphocyte responses in vitro is diminished in infected individuals, and that this may be caused by defects in T cell activation.