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Production by T Cells in Experimental Chagas’ Disease Is Mediated by IL-181
*
Max Planck Institute for Immunobiology and
Department of Pathology, Freiburg, Germany;
Department of Special Zoology and Parasitology, Ruhr-University, Bochum, Germany;
Institute of Immunology, University of Leipzig, Leipzig, Germany;
¶ Department of Immunology, Institut Pasteur, Paris, France; and
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Department of Immunology, University of Cape Town, Cape Town, South Africa
IL-12p35-deficient (IL-12p35-/-) mice were highly
susceptible to Trypanosoma cruzi infection and succumbed
during acute infection, demonstrating the crucial importance of
endogenous IL-12 in resistance to experimental Chagas’ disease.
Delayed immune responses were observed in mutant mice, although
comparable IFN-
and TNF-
blood levels as in wild-type mice were
detected 2 wk postinfection. In vivo and in vitro analysis demonstrated
that T cells, but not NK cells, were recruited to infected organs.
Analysis of mice double deficient in the recombinase-activating gene 2
(RAG2) and IL-12p35, as well as studies involving T cell
depletion, identified CD4+ T cells as the cellular source
for IL-12-independent IFN- production. IL-18 was induced in
IL-12p35-/- mice and was responsible for IFN-
production, as demonstrated by in vivo IL-18 neutralization studies. In
conclusion, evidence is presented for an IL-12-independent IFN-
production in experimental Chagas’ disease that is T cell and IL-18
dependent.
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