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在缺乏γδ T细胞的小鼠中,恰加斯病病情减轻。

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

作者信息

Santos Lima E C, Minoprio P

机构信息

Départment d'Immunologie, Centre National de la Recherche Scientifique URA 1960, Institut Pasteur, Paris, France.

出版信息

Infect Immun. 1996 Jan;64(1):215-21. doi: 10.1128/iai.64.1.215-221.1996.

DOI:10.1128/iai.64.1.215-221.1996
PMID:8557342
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC173748/
Abstract

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.

摘要

通过监测在T细胞受体Cδ基因座破坏后缺乏γδT细胞的小鼠中克氏锥虫感染的进程,评估γδT细胞在恰加斯病免疫病理学中的作用。在感染的急性期和慢性期,比较δ基因敲除小鼠及其同窝小鼠的寄生虫血症水平、淋巴细胞激活状态、淋巴因子产生水平以及组织病理学。虽然两组中循环寄生虫的水平没有显著差异,但γδT细胞缺陷小鼠的死亡率评分以及骨骼肌和心肌的炎性病变数量低于同窝对照。此外,在感染的急性期和慢性期,通过脾脏中增殖活性以及B细胞和T细胞母细胞数量测量的多克隆淋巴细胞激活在缺陷小鼠中降低。从未感染的γδT细胞缺陷小鼠获得的γ干扰素mRNA水平,已知是抵抗克氏锥虫感染的关键淋巴因子,在未感染的γδT细胞缺陷小鼠中显著高于对照动物,并且在急性感染过程中略高于同窝小鼠的水平。然而,有趣的是,在慢性期,两组小鼠中这种淋巴因子的水平在统计学上没有差异。这些结果表明,γδT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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