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恶性疟原虫抗原诱导的增殖以及从疟疾免疫个体分离的淋巴细胞产生白细胞介素-2 。

Proliferation induced by Plasmodium falciparum antigen and interleukin-2 production by lymphocytes isolated from malaria-immune individuals.

作者信息

Theander T G, Bygbjerg I C, Jepsen S, Svenson M, Kharazmi A, Larsen P B, Bendtzen K

出版信息

Infect Immun. 1986 Jul;53(1):221-5. doi: 10.1128/iai.53.1.221-225.1986.

Abstract

Affinity-purified Plasmodium falciparum soluble antigens (SPAg) isolated from in vitro cultures of the parasite were shown to be relatively free of nonspecific polyclonal activators. To determine the presence of lymphocytes with specificity against SPAg in the peripheral blood of malaria-immune individuals, the proliferative response and the interleukin-2 (IL-2) production of SPAg-activated mononuclear cells (MNCs) from individuals unexposed, sensitized, and immune to malaria were measured. It was found that MNC isolated from malaria-immune individuals proliferated in response to SPAg and that this activation resulted in measurable IL-2 production in 5 of 10 MNC cultures. MNC isolates from most unexposed individuals did not respond to SPAg. To establish which cells responded to SPAg, different subpopulations of MNCs were tested. Only T helper cells were found to respond, and they responded only when cocultured with monocytes. The finding of parasite-specific T helper cells in the blood of malaria-immune individuals and the fact that some of these cells were able to produce IL-2 in vitro support the hypothesis that in malaria the cellular part of the protective immune response is initiated by immune T cells. These cells may activate nonspecific effector cells (i.e., macrophages) that eliminate the parasite.

摘要

从疟原虫体外培养物中分离出的经亲和纯化的恶性疟原虫可溶性抗原(SPAg)显示相对不含非特异性多克隆激活剂。为了确定疟疾免疫个体外周血中是否存在对SPAg具有特异性的淋巴细胞,我们检测了未接触过疟疾、已致敏和对疟疾免疫的个体中SPAg激活的单核细胞(MNC)的增殖反应和白细胞介素-2(IL-2)的产生。结果发现,从疟疾免疫个体中分离出的MNC对SPAg有增殖反应,并且这种激活在10个MNC培养物中的5个中导致了可测量的IL-2产生。大多数未接触过疟疾的个体的MNC分离物对SPAg无反应。为了确定哪些细胞对SPAg有反应,我们对MNC的不同亚群进行了测试。结果发现只有辅助性T细胞有反应,并且它们只有在与单核细胞共培养时才有反应。在疟疾免疫个体的血液中发现寄生虫特异性辅助性T细胞,以及其中一些细胞能够在体外产生IL-2这一事实,支持了以下假设:在疟疾中,保护性免疫反应的细胞部分是由免疫T细胞启动的。这些细胞可能激活非特异性效应细胞(即巨噬细胞)来清除寄生虫。

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