Endogenous IL-10 and IFN-gamma production controls thymic cell proliferation in mice acutely infected by Trypanosoma cruzi

• Published in: Scandinavian journal of immunology Vol. 39; no. 1; p. 51
• Main Authors: Leite de Moraes, M D, Minoprio, P, Dy, M, Dardenne, M, Savino, W, Hontebeyrie-Joskowicz, M
• Format: Journal Article
• Language: English
• Published: England 01.01.1994
• Subjects: Animals; Antibodies, Monoclonal; CD3 Complex - immunology; Cells, Cultured; Chagas Disease - immunology; Concanavalin A - immunology; Cytotoxicity, Immunologic - immunology; Disease Models, Animal; Interferon-gamma - biosynthesis; Interleukin-10 - biosynthesis; Lymphocyte Activation - immunology; Mice; Mice, Inbred C57BL; T-Lymphocytes - immunology; T-Lymphocytes, Cytotoxic - immunology; Thymus Gland - cytology; Thymus Gland - immunology
• ISSN: 0300-9475
• DOI: 10.1111/j.1365-3083.1994.tb03339.x

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 cytokine production is modified, with a striking increase in IL-10, IFN-gamma, IL-4, IL-5 and IL-6 production. The results indicate that IL-10 plus IFN-gamma 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-gamma production.