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Chagas' disease is attenuated in mice lacking gamma delta T cells.

机译:在缺乏γ-δT细胞的小鼠中,恰加斯氏病被减弱。

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The role of gamma delta T cells in the immunopathology of Chagas' disease is evaluated by monitoring the course of Trypanosoma cruzi infection in mice lacking gamma delta T cells after disruption of the T-cell receptor C delta locus. Levels of parasitemia, states of lymphocyte activation, and levels of lymphokine production as well as tissue pathology are compared in delta knockout mice and their littermates in acute and chronic phases of infection. Although the levels of circulating parasites do not significantly differ in the two groups, mortality scores and numbers of inflammatory lesions of skeletal and cardiac muscles are lower in gamma delta T cell-deficient m ice than in littermate controls. Furthermore, polyclonal lymphocyte activation, as measured by proliferative activities and numbers of B- and T-cell blasts in the spleen, are reduced in deficient mice in the acute and chronic phases of infection. Levels of gamma interferon mRNA obtained from total spleen cells, known to be a critical lymphokine in resistance to T. cruzi infection, are significantly higher in uninfected gamma delta T cell-deficient mice than in control animals and slightly above levels for littermates in the course of acute infection. Interestingly, however, in chronic phases, the levels of this lymphokine are not statistically different between the two groups of mice. These results indicate that gamma delta T cells do not play a crucial role in parasite clearance during the acute phase of the disease but contribute to the mechanisms leading to tissue damage and pathology.
机译:γδT细胞在恰加斯氏病免疫病理学中的作用是通过监测T细胞受体Cδ基因座破坏后缺乏γδT细胞的小鼠克氏锥虫感染的过程来评估的。比较了在感染的急性和慢性期的三角洲剔除小鼠及其同窝仔中的寄生虫血症水平,淋巴细胞活化状态,淋巴因子产生水平以及组织病理学。尽管两组中循环寄生虫的水平没有显着差异,但γ-δT细胞缺陷型小鼠的死亡率和骨骼和心肌炎性病变的数量均低于同窝对照组。此外,在感染的急性和慢性阶段,缺陷小鼠的多克隆淋巴细胞活化(通过增殖活性和脾脏中B细胞和T细胞胚细胞的数量来衡量)降低了。从总脾细胞获得的γ-干扰素mRNA水平,被认为是对克鲁斯感染的关键淋巴因子,在未感染的γ-δT细胞缺陷小鼠中明显高于对照动物,在此过程中同窝仔的水平略高于急性感染。然而,有趣的是,在慢性期,两组小鼠之间这种淋巴因子的水平在统计学上没有差异。这些结果表明,γ-δT细胞在疾病急性期的寄生虫清除中不发挥关键作用,但有助于导致组织损伤和病理的机制。

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