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Infection and Immunity, March 2004, p. 1397-1401, Vol. 72, No. 3
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.3.1397-1401.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Role of NK Cells and Gamma Interferon in Transplacental Passage of Toxoplasma gondii in a Mouse Model of Primary Infection

Institut de Parasitologie et de Pathologie Tropicale, INSERM U392, 67000 Strasbourg, France

Received 23 September 2003/ Returned for modification 10 November 2003/ Accepted 9 December 2003

Protective immunity in mice infected with Toxoplasma gondii is mainly mediated by NK cells, CD4 and CD8 T cells, and type 1 cytokines, such as gamma interferon (IFN-). To clarify the roles of NK cells and IFN- in protection against primary congenital toxoplasmosis, we used recombination activating gene 2 knockout (RAG-2^-/-) mice, which lack T and B lymphocytes, in comparison with the wild-type BALB/c model. RAG-2^-/- mice had a significantly lower risk of fetal toxoplasmosis than BALB/c mice (25 versus 63.9%; P = 0.003). This protection was associated with an increased number of maternal NK cells, IFN- secretion by spleen cells, and decreased parasitemia. In the RAG-2^-/- mice, NK cell depletion increased both the rate of fetal infection, to 56.5% (P = 0.02), and the blood parasite burden. Conversely, in the BALB/c mice, this treatment did not modify maternofetal transmission or the blood parasite burden. Neutralization of IFN- in both infected RAG-2^-/- and BALB/c mice decreased congenital Toxoplasma transmission, contrasting with an exacerbation of maternal infection. These data suggest that a partially protective immunity against congenital toxoplasmosis is achieved due to the increased number of NK cells in RAG-2^-/- mice. However, it seems that IFN- enhances, directly or indirectly, the transplacental transmission.

Editor: W. A. Petri, Jr.

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