MALARIA PARASITE LIGANDS AND HOST CELL RECEPTORS

疟疾的生命周期涉及受体特异性 这种相互作用允许红细胞的侵入和 感染红细胞到内皮细胞。这些特定事件是潜在的 疫苗和药物干预的目标。我们已经证明 与间日疟原虫侵入红细胞的基序相同， P.发现恶性疟原虫在变异抗原上有2 - 5个拷贝 恶性疟原虫我们正在确定这些图案是否与 粘附于内皮细胞和红细胞形成红细胞， 致病标记变异抗原上的一个结构域 内皮细胞上的CD 36由于大多数寄生虫与CD 36结合， 主要的保护性免疫反应是针对这些变异抗原， 也许有可能开发一种针对这一领域的疫苗， 寄生虫虽然这是违反直觉的（变化的目的是 逃避免疫），该结构域周围的表位可能不 通常诱导免疫，因为它们是隐蔽的，也就是说， 免疫原性，但保护可以诱导后， 预防针我们也在寻找其他的入侵受体 红细胞和附着在内皮细胞上。

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.