In vitro simulation of immunosuppression caused by Trypanosoma brucei.

Macrophage populations derived from Trypanosoma brucei-infected mice suppress both interleukin-2 (IL-2) production and IL-2 receptor (IL-2R) expression. A prostaglandin-independent mechanism accounts for the suppression of IL-2R expression, while the suppression of IL-2 is prostaglandin-dependent. A macrophage hybridoma cell line (i.e. 2C11-12) was used to mimic the parasite-induced immunosuppression in vitro. It was found that 2C11-12 cells acquired a suppressive potential in vitro following interaction with opsonized living parasites. T. brucei-pulsed 2C11-12 cells failed to block IL-2 secretion in the presence of indomethacin but still suppressed the IL-2R expression. In contrast, addition of living T. brucei parasites to the cultures caused a complete suppression of IL-2 secretion and IL-2R expression, even in the presence of indomethacin. Hence, the addition of excess living parasites to the cultures could cause a depression which was different from the suppression associated with infection, whereas the addition of parasite-pulsed 2C11-12 cells mimicked the situation occurring during infection. This model system can be adopted as a suitable tool to unravel the mechanisms underlying the suppression of IL-2R expression during T. brucei infections.