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辅助性T细胞失活后,克氏锥虫感染小鼠的寄生虫负荷增加,心肌炎症减轻。

Parasitic load increases and myocardial inflammation decreases in Trypanosoma cruzi-infected mice after inactivation of helper T cells.

作者信息

Russo M, Starobinas N, Minoprio P, Coutinho A, Hontebeyrie-Joskowicz M

机构信息

Departamento de Immunologia, Universidade de Sao Paulo, Brasil.

出版信息

Ann Inst Pasteur Immunol. 1988 May-Jun;139(3):225-36. doi: 10.1016/0769-2625(88)90136-5.

DOI:10.1016/0769-2625(88)90136-5
PMID:2901844
Abstract

In order to characterize the role played by CD4+ T lymphocytes in the immunopathology of acute Trypanosoma cruzi infection, we compared the numbers of blood and tissue parasites and the heart inflammatory reaction in normal and anti-CD4 antibody-treated C3H mice. Treatment of mice with anti-CD4 mAb during acute infection markedly inhibited T-helper-cell-dependent activities, as measured by peritoneal macrophage activation and immunoglobulin secretion by splenic B lymphocytes. After in vivo inactivation of helper T cells, the number of blood and tissue parasites significantly increased, while the inflammatory cellular infiltrates of heart muscles diminished. Our results indicate that CD4+ T lymphocytes play a dual role in the immunopathology of acute experimental Chagas' disease.

摘要

为了明确CD4 + T淋巴细胞在克氏锥虫急性感染免疫病理学中所起的作用,我们比较了正常C3H小鼠和经抗CD4抗体处理的C3H小鼠血液及组织中的寄生虫数量以及心脏的炎症反应。在急性感染期间用抗CD4单克隆抗体处理小鼠,可显著抑制辅助性T细胞依赖性活动,这可通过腹膜巨噬细胞激活和脾B淋巴细胞免疫球蛋白分泌来衡量。在体内使辅助性T细胞失活后,血液和组织中的寄生虫数量显著增加,而心肌的炎性细胞浸润减少。我们的结果表明,CD4 + T淋巴细胞在急性实验性恰加斯病的免疫病理学中起双重作用。

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Parasitic load increases and myocardial inflammation decreases in Trypanosoma cruzi-infected mice after inactivation of helper T cells.辅助性T细胞失活后,克氏锥虫感染小鼠的寄生虫负荷增加,心肌炎症减轻。
Ann Inst Pasteur Immunol. 1988 May-Jun;139(3):225-36. doi: 10.1016/0769-2625(88)90136-5.
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Experimental infection with Trypanosoma cruzi increases the population of CD8(+), but not CD4(+), immunoglobulin G Fc receptor-positive T lymphocytes.克氏锥虫实验性感染会增加CD8(+)而非CD4(+)免疫球蛋白G Fc受体阳性T淋巴细胞的数量。
Infect Immun. 2005 Aug;73(8):5048-52. doi: 10.1128/IAI.73.8.5048-5052.2005.
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CCR5 plays a critical role in the development of myocarditis and host protection in mice infected with Trypanosoma cruzi.
CCR5在克氏锥虫感染小鼠的心肌炎发展和宿主保护中发挥关键作用。
J Infect Dis. 2005 Feb 15;191(4):627-36. doi: 10.1086/427515. Epub 2005 Jan 13.
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Evidence for a perforin-mediated mechanism controlling cardiac inflammation in Trypanosoma cruzi infection.穿孔素介导机制控制克氏锥虫感染中心脏炎症的证据。
Int J Exp Pathol. 2002 Apr;83(2):67-79. doi: 10.1046/j.1365-2613.2002.00215.x.
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Infect Immun. 2001 Apr;69(4):2252-9. doi: 10.1128/IAI.69.4.2252-2259.2001.
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