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首页> 外文期刊>Infection and immunity >Gamma interferon-dependent temporary resistance to acute Toxoplasma gondii infection independent of CD4+ or CD8+ lymphocytes.
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Gamma interferon-dependent temporary resistance to acute Toxoplasma gondii infection independent of CD4+ or CD8+ lymphocytes.

机译：γ干扰素依赖性的对弓形虫急性感染的临时耐药性，独立于CD4 +或CD8 +淋巴细胞。

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摘要

It is well established that resistance to acute primary Toxoplasma gondii infection is mediated by a gamma interferon (IFN-gamma)-dependent mechanism. The present in vivo experiments were undertaken to investigate the cellular basis for this resistance. We show here that immunocompetent T. gondii-infected C57BL/6 (B6) mice treated with anti-IFN-gamma or with anti-Thy-1 or anti-asialo-GM1 antibodies die sooner than infected mice treated with antibodies that deplete both CD4+ and CD8+ T lymphocytes. Thy-1+ CD4- CD8- cells accumulated in the peritoneal cavities of B6 mice during the early stages of an intraperitoneal infection but did not accumulate in sham-infected control mice, and substantial numbers of Thy-1+ CD4- CD8- cells were recovered from the peritoneal cavities of infected B6 mice treated with antibodies that depleted CD4+ and CD8+ lymphocytes. Depletion of Thy-1+ cells reduced IFN-gamma to undetectable levels, whereas depletion of CD4+ and CD8+ cells did not reduce IFN-gamma levels. Thus T. gondii infection in immunocompetent B6 mice elicits Thy-1+ CD4- CD8- cells which either produce protective IFN-gamma themselves or control its production by other cells. It is likely that the function of these Thy-1+ CD4- CD8- cells is to control T. gondii tachyzoites during the early stages of primary infection before specific CD4(+)- and/or CD8(+)-dependent immunity develops.
机译：公认的是，对急性原发性弓形虫感染的抗性是由γ-干扰素（IFN-γ）依赖性机制介导的。进行本体内实验以研究这种抗性的细胞基础。我们在这里显示，用抗IFN-γ或抗Thy-1或抗亚洲人GM1抗体治疗的具有免疫能力的刚地弓形虫感染的C57BL / 6（B6）小鼠比用同时消耗两种CD4 +的抗体治疗的感染小鼠更快死亡和CD8 + T淋巴细胞。 Thy-1 + CD4-CD8-细胞在腹膜内感染的早期阶段积聚在B6小鼠的腹腔中，但未在假感染的对照小鼠中积聚，并且大量Thy-1 + CD4-CD8-细胞是从用耗尽CD4 +和CD8 +淋巴细胞的抗体处理的受感染B6小鼠的腹膜腔中恢复。 Thy-1 +细胞的耗竭将IFN-γ降至无法检测的水平，而CD4 +和CD8 +细胞的耗竭却未降低IFN-γ的水平。因此，具有免疫能力的B6小鼠中的弓形虫感染会引起Thy-1 + CD4-CD8-细胞，它们本身会产生保护性IFN-γ或控制其他细胞的产生。这些Thy-1 + CD4-CD8-细胞的功能可能是在特定CD4（+）-和/或CD8（+）依赖性免疫发展之前，在原发感染的早期阶段控制刚地弓形虫速殖子。

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