Wright E P, el Amin E R
Department of International Education, Royal Tropical Institute, Amsterdam, The Netherlands.
Biochem Cell Biol. 1989 Sep;67(9):525-36. doi: 10.1139/o89-084.
Infections with Leishmania parasites are initiated by bites from infected sandflies; the injected promastigotes are attacked by phagocytic cells but succeed in entering cells of the macrophage family and surviving in them. The secrets of the success of the extracellular form in penetrating the host cell and of the intracellular form in surviving in a potentially hostile environment are yet to be unraveled. The infectivity of the extracellular promastigote is related to the expression on its surface of molecules that interact with the surface of the host cell. One of these molecules is the promastigote surface protease, or gp63, which is also a dominant surface antigen; this enzyme is thought to be involved in binding to the macrophage via the cell receptors for mannose and fucose and for the third component of complement. Another important surface component is the lipophosphoglycan, consisting of a series of phosphorylated disaccharides linked to a novel lipid anchor in the membrane. This is also released from the parasite surface and was earlier identified as a highly immunogenic antigen excreted into culture medium. It can activate complement and may in this way promote attachment of the parasite to the macrophage. Other surface structures include the acid phosphatase, a glyco-inositol phospholipid, another glycolipid, and membrane proteins of 80 and 17 kilodaltons. All of these may play a role in attachment of the promastigote to the macrophage host cell, as well as in the survival of the amastigote within the macrophage, perhaps by inhibiting the activities of destructive enzymes. The roles in infectivity of these components of the Leishmania surfaces and their interactions with the various receptors on macrophages are discussed. The immune responses induced by these and other parasite antigens during infections in humans and experimental animals are also described briefly, especially those responses that may contribute to protection from infection, or to diagnosis and epidemiology.
利什曼原虫寄生虫感染是由受感染的白蛉叮咬引发的；注入的前鞭毛体受到吞噬细胞攻击，但成功进入巨噬细胞家族的细胞并在其中存活。细胞外形式成功穿透宿主细胞以及细胞内形式在潜在的敌对环境中存活的奥秘尚未解开。细胞外前鞭毛体的感染性与其表面与宿主细胞表面相互作用的分子表达有关。其中一种分子是前鞭毛体表面蛋白酶，即gp63，它也是一种主要的表面抗原；这种酶被认为通过甘露糖、岩藻糖和补体第三成分的细胞受体参与与巨噬细胞的结合。另一个重要的表面成分是脂磷壁酸聚糖，它由一系列磷酸化二糖与膜中的一种新型脂质锚相连组成。它也从寄生虫表面释放出来，较早前被鉴定为分泌到培养基中的一种高度免疫原性抗原。它可以激活补体，并可能以此促进寄生虫与巨噬细胞的附着。其他表面结构包括酸性磷酸酶、糖基磷脂酰肌醇、另一种糖脂以及80和17千道尔顿的膜蛋白。所有这些可能在前鞭毛体与巨噬细胞宿主细胞的附着中发挥作用，以及在巨噬细胞内无鞭毛体的存活中发挥作用，也许是通过抑制破坏酶的活性。讨论了利什曼原虫表面这些成分在感染性中的作用及其与巨噬细胞上各种受体的相互作用。还简要描述了这些和其他寄生虫抗原在人类和实验动物感染期间诱导的免疫反应，特别是那些可能有助于预防感染、诊断和流行病学的反应。
