Perlmann P, Troye-Blomberg M
Department of Immunology, Stockholm University, Sweden.
Folia Biol (Praha). 2000;46(6):210-8.
Malaria is caused by the protozoon Plasmodium, transmitted to humans by Anopheles mosquitoes. The most dangerous of the plasmodia infecting humans is Plasmodium falciparum. The disease is caused by those parasite stages which multiply asexually in red blood cells. In non-immune individuals, P. falciparum may cause severe and life-threatening disease. Another risk group is constituted by pregnant women, particularly during their first pregnancies. Immunity to malaria usually requires repeated exposure to the parasite to become long lasting. One reason for this is the capacity of the parasite to vary the antigens which are major targets for protective antibodies. Antibody-dependent protection is primarily mediated by cytophilic IgG antibodies activating cytotoxic and phagocytic effector functions of neutrophils and monocytes. Malaria infection also involves elevated production of IgE antibodies. However, IgE-containing immune complexes are pathogenic rather than protective by crosslinking IgE receptors (CD23) on monocytes, leading to local overproduction of TNF, a major pathogenic factor in this disease. T cells are essential for both acquisition and regulation of malaria immunity. The major T cells controlling blood stage infections are CD4+ of both the Thl and Th2 subsets. However, T cells carrying the gamma6 receptor also contribute to this control. The balance between the cytokines produced by different cell types is critical for the course of infection, with IFN-gamma having a key role in anti-malaria defence. Blood-stage infections are also under complex genetic control. Among the regulatory genes, those involved in elevated production of TNF are associated with increased risk of severe disease and death due to P. falciparum infection.
疟疾由疟原虫属原生动物引起，通过按蚊传播给人类。感染人类的疟原虫中最危险的是恶性疟原虫。该疾病由在红细胞中进行无性繁殖的寄生虫阶段引起。在非免疫个体中，恶性疟原虫可能导致严重的、危及生命的疾病。另一个风险群体是孕妇，尤其是在她们首次怀孕期间。对疟疾的免疫力通常需要反复接触寄生虫才能持久。原因之一是寄生虫能够改变作为保护性抗体主要靶点的抗原。抗体依赖性保护主要由嗜细胞性IgG抗体介导，这些抗体激活中性粒细胞和单核细胞的细胞毒性和吞噬效应功能。疟疾感染还涉及IgE抗体的产生增加。然而，含IgE的免疫复合物通过交联单核细胞上的IgE受体（CD23）具有致病性而非保护性，导致TNF局部过度产生，TNF是该疾病的主要致病因素。T细胞对于疟疾免疫力的获得和调节都至关重要。控制血液阶段感染的主要T细胞是Th1和Th2亚群的CD4+细胞。然而，携带γ6受体的T细胞也有助于这种控制。不同细胞类型产生的细胞因子之间的平衡对于感染过程至关重要，其中IFN-γ在抗疟疾防御中起关键作用。血液阶段感染也受到复杂的基因控制。在调节基因中，那些参与TNF产生增加的基因与恶性疟原虫感染导致的严重疾病和死亡风险增加有关。
