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抗原特异性CD8 + T细胞克隆可保护小鼠免受急性弓形虫感染。

Antigen-specific CD8+ T cell clone protects against acute Toxoplasma gondii infection in mice.

作者信息

Khan I A, Ely K H, Kasper L H

机构信息

Department of Microbiology, Dartmouth Medical School, Hanover, NH 03756.

出版信息

J Immunol. 1994 Feb 15;152(4):1856-60.

PMID:7907106
Abstract

Encephalitis caused by the obligate intracellular protozoan, Toxoplasma gondii, is a major cause of morbidity and mortality in those afflicted with AIDS. The cell-mediated response is critical for host immunity against this parasite. A panel of T cell clones that proliferate in response to a major parasite protein, p30 (SAG-1) were isolated from mice. One of these clones (C3) bearing the CD8+ phenotype was able to induce nearly 100% protection against acute infection when adoptively transferred into naive mice. In contrast, an Ag-specific CD4+ T cell clone (C2) failed to show significant protection in spite of its ability to produce similar quantities of IFN-gamma. Depletion of host CD4+ T cells with mAb had no effect on CD8(+)-mediated adoptive protection, whereas treatment with anti-IFN-gamma completely abrogated this protection. These results indicate that Ag-specific CD8+ T cells in combination with IFN-gamma are able to induce significant protection against acute toxoplasmosis in the experimental murine model.

摘要

由专性细胞内原生动物刚地弓形虫引起的脑炎,是艾滋病患者发病和死亡的主要原因。细胞介导的反应对于宿主抵抗这种寄生虫的免疫力至关重要。从小鼠中分离出一组响应主要寄生虫蛋白p30(SAG-1)而增殖的T细胞克隆。这些克隆之一(C3)具有CD8 +表型,当将其过继转移到未感染的小鼠中时,能够诱导对急性感染的近100%的保护作用。相比之下,尽管Ag特异性CD4 + T细胞克隆(C2)能够产生相似量的IFN-γ,但其未能显示出明显的保护作用。用单克隆抗体耗尽宿主CD4 + T细胞对CD8(+)介导的过继保护没有影响,而用抗IFN-γ治疗则完全消除了这种保护作用。这些结果表明,Ag特异性CD8 + T细胞与IFN-γ联合能够在实验性小鼠模型中诱导对急性弓形虫病的显著保护作用。

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