Ropert C, Gazzinelli R T
Centro de Pesquisas René Rachou, FIOCRUZ, Belo Horizonte, MG, Brazil.
Curr Opin Microbiol. 2000 Aug;3(4):395-403. doi: 10.1016/s1369-5274(00)00111-9.
Glycosylphosphatidylinositol (GPI) anchor and glycoinositolphospholipid (GIPL) are abundant molecules present in the membrane of parasitic protozoa that are common etiologic agents of medical and veterinary diseases. Recent studies have documented the immunostimulatory/regulatory activity of protozoan-derived GPI-anchors and related structures. Among the bioactivity displayed by the protozoan-derived GPI-anchor is the ability to elicit the synthesis of pro-inflammatory cytokines as well as nitric oxide by host macrophages. In contrast, at high concentrations GIPL and lipophosphoglycan (LPG) derived from protozoan parasites suppress several functions of the host immune system. Additionally, the protozoan-derived GPI-anchor and GIPL have been shown to serve as targets for both specific B and NK-T lymphocyte responses. This information extends our knowledge about parasite molecules that stimulate/regulate the host immune system during protozoan infection. The identification of receptor(s) and signaling pathways triggered by these GPI-related glycolipids may provide new insights for the development of therapies that inhibit detrimental immune responses or potentiate beneficial immune responses observed during infection with protozoan parasites.
糖基磷脂酰肌醇（GPI）锚和糖肌醇磷脂（GIPL）是寄生原生动物膜中丰富的分子，这些原生动物是医学和兽医学疾病的常见病原体。最近的研究记录了原生动物来源的GPI锚和相关结构的免疫刺激/调节活性。原生动物来源的GPI锚所展现的生物活性之一是能够诱导宿主巨噬细胞合成促炎细胞因子以及一氧化氮。相比之下，原生动物寄生虫来源的高浓度GIPL和脂磷壁酸（LPG）会抑制宿主免疫系统的多种功能。此外，原生动物来源的GPI锚和GIPL已被证明是特异性B淋巴细胞和自然杀伤T淋巴细胞反应的靶点。这些信息扩展了我们对原生动物感染期间刺激/调节宿主免疫系统的寄生虫分子的认识。鉴定由这些与GPI相关的糖脂触发的受体和信号通路，可能为开发抑制有害免疫反应或增强原生动物寄生虫感染期间观察到的有益免疫反应的疗法提供新的见解。
