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The induction of a type 1 immune response following a Trypanosoma brucei infection is MyD88 dependent
被引:107
作者:

Drennan, MB
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机构: Vrije Univ Brussels VIB, Dept Cellular & Mol Interact, Lab Cellular & Mol Immunol, Brussels, Belgium

Stijlemans, B
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机构: Vrije Univ Brussels VIB, Dept Cellular & Mol Interact, Lab Cellular & Mol Immunol, Brussels, Belgium

Van Den Abbeele, J
论文数: 0 引用数: 0
h-index: 0
机构: Vrije Univ Brussels VIB, Dept Cellular & Mol Interact, Lab Cellular & Mol Immunol, Brussels, Belgium

Quesniaux, VJ
论文数: 0 引用数: 0
h-index: 0
机构: Vrije Univ Brussels VIB, Dept Cellular & Mol Interact, Lab Cellular & Mol Immunol, Brussels, Belgium

Barkhuizen, M
论文数: 0 引用数: 0
h-index: 0
机构: Vrije Univ Brussels VIB, Dept Cellular & Mol Interact, Lab Cellular & Mol Immunol, Brussels, Belgium

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De Baetselier, P
论文数: 0 引用数: 0
h-index: 0
机构: Vrije Univ Brussels VIB, Dept Cellular & Mol Interact, Lab Cellular & Mol Immunol, Brussels, Belgium

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Magez, S
论文数: 0 引用数: 0
h-index: 0
机构: Vrije Univ Brussels VIB, Dept Cellular & Mol Interact, Lab Cellular & Mol Immunol, Brussels, Belgium
机构:
[1] Vrije Univ Brussels VIB, Dept Cellular & Mol Interact, Lab Cellular & Mol Immunol, Brussels, Belgium
[2] CNRS, F-45071 Orleans, France
[3] Inst Trop Med, Unit Entomol, B-2000 Antwerp, Belgium
[4] Univ Cape Town, Immunol Infect Dis Med Res Council, Inst Infect Dis & Mol Med, Fac Hlth Sci,Univ Cape Town Unit, ZA-7925 Cape Town, South Africa
基金:
英国惠康基金;
关键词:
D O I:
10.4049/jimmunol.175.4.2501
中图分类号:
R392 [医学免疫学];
Q939.91 [免疫学];
学科分类号:
100102 ;
摘要:
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-gamma 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-gamma 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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页码:2501 / 2509
页数:9
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