Endogenous IL‐10 and IFN‐γ Production Controls Thymic Cell Proliferation in Mice Acutely Infected by Trypanosoma cruzi

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Abstract
Thymocytes from mice with experimental Trypanosoma cruzi infection respond poorly to Con‐A stimulation. However, the proliferative capacity of these cells is not impaired, as demonstrated by the fact that at high doses, exogenous rIL‐2 restores thymidine uptake. This finding could be explained either by insufficient IL‐2 production or by the appearance of inhibitory factors during T. cruzi infection. This paper shows that in response to Con A, IL‐2 production is decreased in the model. Furthermore, the whole profile of cylokine production is modified, with a striking increase in IL‐10, IFN‐γ, IL‐4, IL‐5 and IL‐6 production. The results indicate that IL‐10 it plus IFN‐γ are responsible for the decrease in the Con A induced proliferation since a normal proliferative response as well as normal IL‐2 production can be restored if both cytokines are neutralized by adding their monoclonal antibodies (MoAbs). Evidence is provided also for an enhanced non‐specific cytotoxicity of thymic cells from infected mice that might involve IL‐4, IL‐5 and IL‐6. This is the first study demonstrating an alteration of thymic cell function by T. cruzi infection which results from overstimulation of IL‐10 and IFN‐γ production.