Suppressor macrophages in Trypanosoma brucei infection: nitric oxide is related to both suppressive activity and lifespan in vivo

摘要: SUMMARY African trypanosome infections cause immunosuppression in both experimental rodent and natural hosts. One characteristic of this is an eliciting suppressor macrophages which results unresponsiveness lymphocytes. Macrophages from Trypanosoma brucei-infected mice have previously been shown to produce high levels nitric oxide (NO). Using model systems based on vivo macrophage transfer drug cure, we sought determine the relationship between NO suppressed lymphocyte responses. Peritoneal T. inhibited Concanavalin A (Con-A) response spleen cells syngeneic recipients 3–4 days after due activity macrophages. When synthesis was either vitro or suppressive effects were partially abrogated. These data provide evidence a role for mediating during murine brucei infection. Suppression spleens receiving transient, with total recovery cell mitogen responses six transfer. found coincide presence absence (respectively) donor recipient spleens. treated curative dose trypanocide there followed responsiveness period 4–5 days, directly correlated reduction control vitro. The apparent loss 4–6 cured animals be NO-mediated apoptosis these cells.