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* Immunology of Infectious Disease Medical Research Council/University of Cape Town Unit, Institute of Infectious Disease and Molecular Medicine, Health Science Faculty, University of Cape Town, Cape Town, South Africa;
Department of Cellular and Molecular Interactions, Vlaams Interuniversitair Instituut voor Biotechnologie, Laboratory of Cellular and Molecular Immunology, Vrije Universiteit Brussels, Brussels, Belgium;
Centre National de la Recherché Scientifique, Molecular Immunology and Embryology, Orléans, France; and
Unit of Entomology, Institute of Tropical Medicine, Antwerp, Belgium
The initial host response toward the extracellular parasite Trypanosoma brucei is characterized by the early release of inflammatory mediators associated with a type 1 immune response. In this study, we show that this inflammatory response is dependent on activation of the innate immune system mediated by the adaptor molecule MyD88. In the present study, MyD88-deficient macrophages are nonresponsive toward both soluble variant-specific surface glycoprotein (VSG), as well as membrane-bound VSG purified from T. brucei. Infection of MyD88-deficient mice with either clonal or nonclonal stocks of T. brucei resulted in elevated levels of parasitemia. This was accompanied by reduced plasma IFN-
and TNF levels during the initial stage of infection, followed by moderately lower VSG-specific IgG2a Ab titers during the chronic stages of infection. Analysis of several TLR-deficient mice revealed a partial requirement for TLR9 in the production of IFN- and VSG-specific IgG2a Ab levels during T. brucei infections. These results implicate the mammalian TLR family and MyD88 signaling in the innate immune recognition of T. brucei.
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