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Virulent Toxoplasma gondii strain RH promotes T-cell-independent overproduction of proinflammatory cytokines IL12 and -interferon

^1,2,3Microbiology Unit, Cliniques Universitaires Saint-Luc¹ and Experimental Medicine Unit², Christian de Duve Institute of Cellular Pathology, Catholic University of Louvain and Ludwig Institute for Cancer Research³, Brussels, Belgium ⁴Laboratory Immunobiol, REGA Institute, K. U. Leuven, Belgium ⁵Gastroenterology Division, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA ⁶Wyeth Inc., Cambridge, MA 02140, USA

Correspondence J.-P. Coutelier coutelier{at}mexp.ucl.ac.be

Received December 21, 2001
Accepted May 27, 2003

The aim of this study was the analysis of the cytokine response in BALB/c mice infected with the highly virulent RH or the weakly virulent Beverley strains of Toxoplasma gondii. Analysis of cytokine messages showed increased expression of IL12, IFN- and TNF-, but not IL4 mRNAs in spleen cells after infection with the T. gondii strains RH and Beverley. High levels of circulating IL12 and IFN- were detected in the serum of mice infected with strain RH, although TNF- levels remained low. In contrast, the same cytokines were detected at only low levels in the serum of mice infected with the Beverley strain. Administration of antibody against IL12 or IFN- significantly delayed time to death of mice infected with strain RH compared to controls. T-Cell-deficient as well as normal mice were equally infected by strain RH, suggesting that T lymphocytes do not contribute to the response. Depletion of natural killer cells from the splenocyte population abolished the in vitro production of IFN-. Together, our data suggest that the virulent strain RH induces in BALB/c mice a type 1 cytokine pattern with T-cell-independent overproduction of IL12 and IFN- that may be involved in the pathogenesis of this micro-organism.

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