Arsić-Arsenijević Valentina, Dzamić Aleksandar, Mitrović Sanja, Radonjić Ivana, Kranjcić-Zec Ivana
Institut za mikrobiologiju i imunologiju, Medicinski fakultet, Beograd.
Med Pregl. 2003 Nov-Dec;56(11-12):557-63. doi: 10.2298/mpns0312557a.
When protozoa enter the blood stream or tissues they can often survive and replicate because they adapt to the resisting natural host defenses. The interaction of immune system with infectious organisms is a dynamic interplay of host mechanisms aimed at eliminating infections and microbial strategies designed to permit survival in the face of powerful effector mechanisms. Protozoa cause chronic and persistent infections, because natural immunity against them is weak and because protozoa have evolved multiple mechanisms for evading and resisting specific immunity.
Different protozoa vary greatly in their structural and biochemical properties and stimulate distinct patterns of immune responses and have evolved unique mechanisms for evading specific immunity. Protozoa activate quite distinct specific immune responses, which are different from the responses to fungi, bacteria and viruses. Protozoa may be phagocytozed by macrophages, but many are resistant to phagocytic killing and may even replicate within macrophages. T. brucei gambiense is the best example of protozoa which can induce humoral immune response because of its extra-cellular location. In Leishmania sp. infections, cellular defense mechanisms depend upon CD4+ T-lymphocytes and activate macrophages as effector cells that are regulated by cytokines of Th1 subset. Plasmodium sp. is a protozoa which show the diversity of defence mechanisms which can be cellular or humoral, depending on Ag and protozoa's location.
Different protozoa have developed remarkably effective ways of resisting specific immunity: a) anatomic sequestration is commonly observed with protozoa Plasmodium and T. gondii; b) some protozoa can become resistant to immune effector mechanisms: Trypanosoma, Leishmania and T. gondii; c) some protozoa have developed effective mechanisms for varying their surface antigens: Plasmodium and Trypanosoma; d) some protozoa shed their antigen coats, either spontaneously or after binding with specific antibodies: E. histolytica; e) some protozoa alter host immune response by nonspecific and generalized immunosuppression (abnormalities in cytokine production, deficient T cell activation): Trypanosoma, Leishmania, Toxoplasma, Entamoeba.
Protozoa activate numerous, different immune mechanisms in human body. Evolution, progression and outcome of diseases depend upon these mechanisms. Resent progresses in research have defined and selected Ag as candidates for new vaccines. Better definitions regarding the role of cytokines in protozoan infections will facilitate rational development of cytokines and cytokine antagonists and their use as immunotherapeutic agents.
当原生动物进入血流或组织时，它们常常能够存活并繁殖，因为它们能适应宿主的天然防御机制。免疫系统与感染性生物体之间的相互作用是宿主旨在消除感染的机制与微生物为在强大的效应机制面前存活而设计的策略之间的动态相互作用。原生动物会引发慢性和持续性感染，这是因为针对它们的天然免疫力较弱，且原生动物已进化出多种逃避和抵抗特异性免疫的机制。
不同的原生动物在结构和生化特性上差异很大，会刺激不同模式的免疫反应，并且进化出了独特的逃避特异性免疫的机制。原生动物激活的特异性免疫反应与对真菌、细菌和病毒的反应截然不同。原生动物可能会被巨噬细胞吞噬，但许多原生动物对吞噬性杀伤具有抗性，甚至可能在巨噬细胞内繁殖。布氏冈比亚锥虫是由于其细胞外定位而能诱导体液免疫反应的原生动物的最佳例子。在利什曼原虫感染中，细胞防御机制依赖于CD4 + T淋巴细胞，并激活巨噬细胞作为效应细胞，这些效应细胞受Th1亚群细胞因子的调节。疟原虫是一种原生动物，其防御机制具有多样性，可根据抗原和原生动物的位置表现为细胞免疫或体液免疫。
不同的原生动物已开发出非常有效的抵抗特异性免疫的方法：a）疟原虫和弓形虫等原生动物通常会出现解剖学隔离；b）一些原生动物可对免疫效应机制产生抗性：如锥虫、利什曼原虫和弓形虫；c）一些原生动物已开发出改变其表面抗原的有效机制：疟原虫和锥虫；d）一些原生动物会自发地或在与特异性抗体结合后脱落其抗原外衣：溶组织内阿米巴；e）一些原生动物通过非特异性和全身性免疫抑制（细胞因子产生异常、T细胞激活不足）改变宿主免疫反应：锥虫、利什曼原虫、弓形虫、溶组织内阿米巴。
原生动物在人体中激活众多不同的免疫机制。疾病的演变、进展和结果取决于这些机制。最近的研究进展已确定并选择抗原作为新型疫苗的候选物。对细胞因子在原生动物感染中作用的更清晰定义将有助于合理开发细胞因子和细胞因子拮抗剂，并将它们用作免疫治疗剂。
