Troye-Blomberg M, Perlmann P, Mincheva Nilsson L, Perlmann H
Department of Immunology, Arrhenius Laboratories F5, Stockholm University, Sweden.
Parassitologia. 1999 Sep;41(1-3):131-8.
The immune mechanisms whereby malaria parasites are eliminated by the human host or how they may avoid the immune response are poorly understood. Individuals living in malaria-endemic areas gradually acquire immunity. It is well established that this immunity involves both cell-mediated and humoral mechanisms and that T cells are the major regulators in both these events. The existence of functionally distinct P. falciparum-specific CD4+ T-cell subsets in humans has been shown in several studies. However, in contrast to what is the case in murine models there is no definitive link between the activation of various T cells and the course of human P. falciparum blood-stage infection. In the present paper we will review recent findings which illustrate how the balance between functionally different T-cell subsets affects the development of malaria immunity but also may contribute to its pathogenicity. An example of the latter is the deposition of IgE-containing immune complexes in small vessels, probably leading to local overproduction of tumor-necrosis factor (TNF), a pathogenic factor in malaria.
人类宿主清除疟原虫的免疫机制，或者它们如何逃避免疫反应，目前还知之甚少。生活在疟疾流行地区的个体逐渐获得免疫力。众所周知，这种免疫力涉及细胞介导和体液机制，并且T细胞是这两种机制的主要调节因子。多项研究表明，人类存在功能不同的恶性疟原虫特异性CD4 + T细胞亚群。然而，与鼠模型不同的是，各种T细胞的激活与人类恶性疟原虫血液阶段感染的病程之间没有明确的联系。在本文中，我们将综述最近的研究结果，这些结果表明功能不同的T细胞亚群之间的平衡如何影响疟疾免疫力的发展，但也可能导致其致病性。后者的一个例子是含IgE免疫复合物在小血管中的沉积，这可能导致肿瘤坏死因子（TNF）在局部过度产生，TNF是疟疾中的一种致病因子。
