Interleukin-10 does not contribute to the pathogenesis of a virulent strain of Toxoplasma gondii

被引:25
|
作者
Wille, U
Villegas, EN
Striepen, B
Roos, DS
Hunter, CA
机构
[1] Univ Penn, Sch Vet Med, Dept Pathobiol, Philadelphia, PA 19104 USA
[2] Univ Georgia, Dept Cellular Biol, Athens, GA 30602 USA
[3] Univ Penn, Dept Biol, Philadelphia, PA 19104 USA
关键词
Toxoplasma gondii; IL-10; GFP-labelled tachyzoites;
D O I
10.1046/j.1365-3024.2001.00389.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Interleukin (IL)-10 is an inhibitor of cell mediated immunity and an antagonist of the development of protective immune responses associated with resistance to T. gondii. These observations led to the hypothesis that the production of IL-10 could contribute to the ability of T. gondii to replicate and survive in an immune competent host. To determine whether the production of IL-10 affects the ability of the RH strain of T. gondii to cause a lethal infection in mice, we compared the immune response to RH in IL-10(+/+) and IL-10(-/-) BALB/c mice. Both groups of mice produced comparable amounts of IL-12 and interferon (IFN)-gamma and had similar mortality curves and parasite burdens. The use of green fluorescent protein-labelled parasites allowed us to infect IL-10(+/+) and IL-10(-/-) mice and use a fluorescence-activated cell sorter to distinguish infected and uninfected populations of macrophages and compare their expression of CD80, CD86 and major histocompatibility complex (MHC) class II. Although infected cells expressed higher overall levels of these molecules than uninfected cells, there were no differences between cells isolated from IL-10(+/+) and IL-10(-/-) mice. Taken together these results indicate that IL-10 is not required for the virulence of the RH strain of T. gondii, nor is it involved in the regulation of the CD80, CD86 and MHC class II molecules during RN-infection.
引用
收藏
页码:291 / 296
页数:6
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