MALARIA PARASITE LIGANDS AND HOST CELL RECEPTORS

疟疾的生命周期涉及受体特异性 允许红细胞入侵和附着的相互作用 感染了红细胞的内皮细胞。这些特定的事件是潜在的 疫苗和药物干预的目标。我们已经证明了 间日疟原虫和间日疟原虫入侵红细胞所涉及的相同基序 恶性疟原虫在变种抗原上有2到5个拷贝。 恶性疟原虫。我们正在确定这些图案是否与 黏附于内皮细胞和红细胞以形成花环，a 致病标志物。变异抗原上的一个结构域与 内皮细胞表面CD36的表达。由于大多数寄生虫结合CD36和 主要的保护性免疫反应是对这些变异抗原的，它 有可能开发一种针对该领域的疫苗 寄生虫。尽管这是违反直觉的(变体旨在 逃脱免疫)，这个区域周围的表位可能不会 通常会诱导免疫力，因为它们是隐蔽的，即不是 在感染过程中具有免疫原性，但在感染后可诱导保护 接种疫苗。我们也在寻找其他的入侵受体 红血球和内皮细胞的附着。

The life cycle of malaria involves receptor-specific interactions that allow invasion of red cells and attachment of infected red cells to endothelium. These specific events are potential targets for vaccines and drug interventions. We have demonstrated that the same motif involved in invading red cells for P. vivax and P. falciparum is found as two to five copies on the variant antigen of P. falciparum. We are determining if these motifs are involved in adhesion to endothelium and to red cells to form rosettes, a pathogenic marker. One of the domains on the variant antigen binds to CD36 on endothelium. As most parasites bind CD36 and the major protective immune response is to these variant antigens, it may be possible to develop a vaccine against this domain on the parasite. Although this is counterintuitive (variation is designed to escape immunity), the epitopes around this domain may not normally induce immunity because they are cryptic, that is, not immunogenic during infection, but protection can be induced after vaccination. We are also searching for other receptors for invasion of red cells and attachment to endothelium.