介白素IL-4以及IL-10之結合效應抑制組織胞漿菌感染中第一型輔助性T細胞之產生而不改變其極性

The Combined Effect of IL-4 and IL-10 Suppresses the Generation of, But Does Not Change, the Polarity of Type-1 T Cells in Histoplasma Infection

彭榮桂(Jung-Kuei Peng)

指導教授 ： 伍安怡

國立臺灣大學/醫學院/免疫學研究所/碩士(2004年)

https://doi.org/10.6342/NTU.2004.01097

摘要

在小鼠的全身性組織胞漿菌炎感染模式中會誘發強烈之第一型細胞激素產生，我們利用此模式來探討在組織胞漿菌感染之免疫反應中，若在第一型T細胞priming階段存在第二型拮抗型細胞激素介白素(IL-4，IL-10)下會否改變第一型T細胞之極性。小鼠在感染組織胞漿菌之前先注射二劑山羊抗鼠IgD免疫球蛋白血清(G

關鍵字

組織胞漿菌炎 ； 第一型第二型免疫反應 ； 干擾素

並列摘要

Dominant type-1 cytokine production is induced in a murine model of systemic histoplasmosis. We used this model to investigate whether the presence of antagonistic cytokines during T cell priming changes the polarity of T cells in response to Histoplasma infection. Before infection with Histoplasma capsulatum, mice were injected twice with goat anti-mouse IgD antiserum (GaMd), which induced expression of dominant type-2 cytokines. At days 7 and 14 after infection, the GaMd-treated mice had suppressed IFN-g response and a significantly greater fungal burden in their spleens and lungs. The number of IFN-g-producing cells as well as the level of IFN-g produced per cell was greatly reduced. Not only CD4+ T cells but also CD8+ T cells were affected. Reduction of IFN-g-producing T cells is not a result in T cell expansion, T cell death, or intrinsic defect in TCR signaling. There was no difference in the numbers of CD4 and CD8 T cells in infected mice with or without GaMd treatment. The number of Histoplasma-induced IFN-g-producing cells was partially restored in GaMd-treated IL-4-/- and IL-10-/- mice and completely restored in IL-4-/-IL-10-/- mice. Thus, the combined effect of IL-4 and IL-10 suppressed the generation of IFN-g-producing cells. A longitudinal study demonstrated that as IL-4 and IL-10 decreased, the number of Histoplasma-induced IFN-g-producing cells rapidly increased, and fungal clearance improved, demonstrating that the presence of IL-4 and IL-10 did not permanently change the polarity of T cells.

並列關鍵字

Histoplasmosis ； Type-1 and type-2 immune response ； interferon

參考文獻

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