Suppressor activity in Leishmania donovani-infected hamster serum: reversion by delipidated bovine serum albumin and role in cell cycle events.

Visceral leishmaniasis, caused by Leishmania donovani, is a chronic disease with a high mortality rate. This protozoan induces a serious dysfunction of the immune system characterized by suppression of the cellular response to parasite antigens. We provide evidence for the involvement of lipids in the immunological alterations of experimental leishmaniasis. Sera obtained from 60-day-infected hamsters present increased triglyceride levels. Inhibition of cell proliferation was observed when splenocytes from normal hamsters were stimulated with concanavalin A in the presence of 3% infected hamster serum (IHS) (Control 50 +/- 3 (x10(3)) cpm; IHS 5 +/- 1 (x10(3)) cpm). This inhibition was reversed by the addition of 5 mg/ml of delipidated bovine serum albumin (BSA) to the cultures (Control 65 +/- 1 (x10(3)) cpm; IHS 75 +/- 3 (x10(3)) cpm). The inhibitory effect of IHS was demonstrable only when added to the culture simultaneously with the mitogen. This effect was not as intense on fresh, pre-activated cells or on the CTLL-2 cells. This cell line stimulated by IL-2 in the presence of IHS is only marginally inhibited (about 20% inhibition). The suppressor effect on CTLL-2 was not reversed by the addition of increasing doses of IL-2 (up to 100 U/ml) to cultures. The inhibition of the proliferative response of the CTLL-2 cells caused by IHS was also reversed by the addition of delipidated BSA. Our data suggest a role for fatty acids in the infected hamster serum-induced suppression of normal or L. donovani-infected cell proliferation.