[Use a of DNA probe to detect cellular immunity against intracellular parasitism].

A Ferreira
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Abstract

By using a specific, repetitive DNA probe, we have been able to detect picograms of P. berghei DNA. With this probe we have determined that: a) P. berghei, inoculated into Norway Brown rats, reaches its peak of proliferation in the liver 44 h after infection; b) gamma interferon inhibits in a dose-dependent fashion the development of liver exoerythrocytic forms (EEF) in vivo and in vitro, and; c) endogenous gamma interferon inhibits the development of EEF in hosts immunized with irradiated sporozoites. Related with and derived from these findings, we have found that, in order to obtain an effective immunity against malaria in experimental animal models, effector mechanisms mediated by T cells are required. This is substantiated by the following facts: a) immune hosts inoculated with monoclonal antibodies against gamma interferon reversed their immunity against a sporozoite challenge; b) This immunity was also reversed when the animals were depleted from their CD8 positive cytotoxic T cells. Therefore, sterile immunity against this parasite requires not only the presence of antibodies but also the inhibition of the EEF by gamma interferon with participation of CD8 positive T cells.

[利用DNA探针检测细胞对细胞内寄生的免疫]。
通过使用一种特殊的、重复的DNA探针,我们已经能够检测到柏氏假体DNA的图形。通过这种探针,我们确定:a)接种挪威褐大鼠的伯氏假体在感染后44 h达到肝脏增殖高峰;b) γ干扰素在体内和体外以剂量依赖的方式抑制肝外红细胞形式(EEF)的发展;c)内源性γ干扰素抑制辐照孢子子免疫的宿主EEF的发育。根据这些发现,我们发现,为了在实验动物模型中获得对疟疾的有效免疫,需要T细胞介导的效应机制。以下事实证实了这一点:a)接种了γ干扰素单克隆抗体的免疫宿主对孢子虫攻击的免疫逆转;b)当动物的CD8阳性细胞毒性T细胞被耗尽时,这种免疫也被逆转。因此,针对这种寄生虫的无菌免疫不仅需要抗体的存在,还需要γ干扰素在CD8阳性T细胞的参与下抑制EEF。
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