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首页> 外文期刊>Infection and immunity >T cells and macrophages in Trypanosoma brucei-related glomerulopathy.
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T cells and macrophages in Trypanosoma brucei-related glomerulopathy.

机译：布氏锥虫相关肾小球病中的T细胞和巨噬细胞。

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In a previous study, susceptibility for Trypanosoma brucei-related glomerulopathy in mice was shown to be dependent on non-major histocompatibility complex genes. Glomerular disease in this model could not be explained by the production of autoantibodies alone. In order to analyze which part of the defense system, in addition to the B-cell compartment, is involved in the development of this infection-related glomerular disease, groups of athymic (BALB/c rnu/rnu), splenectomized, or macrophage-depleted BALB/c mice were inoculated with T. brucei parasites. Polyclonal B-cell activation, invariably observed in infected BALB/c mice, was absent in BALB/c rnu/rnu mice. Glomerular disease in athymic mice, however, as defined by albuminuria and deposition of immune complexes, was not different from that seen in euthymic infected BALB/c mice. Splenectomy prior to inoculation of parasites led to a decreased incidence of albuminuria in 40% of the animals, whereas splenectomy 21 days after inoculation reduced albuminuria significantly, suggesting a role for spleen cells in the induction of glomerular disease. After macrophage depletion with liposome-encapsulated dichlorodimethylene-diphosphonate, infected BALB/c mice developed significantly higher albuminuria levels for a period up to 2 weeks after depletion. Therefore, it was concluded that the development of T. brucei-related glomerular disease is independent of thymus-matured T cells, while the involvement of macrophages in the development of proteinuria is inhibitory rather than disease inducing. Spleen cells other than thymus-dependent T cells, B cells, and macrophages should be investigated for their role in the pathogenesis of this glomerulopathy.
机译：在先前的研究中，小鼠布鲁氏锥虫相关性肾小球病的易感性依赖于非主要组织相容性复合基因。该模型中的肾小球疾病不能仅通过自身抗体的产生来解释。为了分析防御系统的哪一部分，除了B细胞区隔，还参与了与感染相关的肾小球疾病的发展，无胸腺（BALB / c rnu / rnu），脾切除或巨噬细胞-将贫血的BALB / c小鼠接种布鲁氏杆菌寄生虫。在感染的BALB / c小鼠中始终观察到的多克隆B细胞活化在BALB / c rnu / rnu小鼠中不存在。然而，如蛋白尿和免疫复合物的沉积所定义，无胸腺小鼠的肾小球疾病与感染了正常胸腺的BALB / c小鼠没有区别。接种寄生虫前的脾切除术导致40％的动物蛋白尿减少，而接种后21天的脾切除术显着降低了蛋白尿，表明脾细胞在诱导肾小球疾病中发挥了作用。用脂质体包封的二氯二亚甲基-二膦酸酯耗尽巨噬细胞后，感染的BALB / c小鼠在耗尽后长达2周的时间内会出现明显更高的蛋白尿水平。因此，可以得出结论，布鲁氏杆菌相关肾小球疾病的发展与胸腺成熟的T细胞无关，而巨噬细胞参与蛋白尿的发展是抑制性疾病，而不是疾病诱导性疾病。除胸腺依赖性T细胞，B细胞和巨噬细胞外，应研究脾细胞在这种肾小球病发病机理中的作用。

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