期刊
MICROCIRCULATION
卷 11, 期 7, 页码 559-576出版社
WILEY
DOI: 10.1080/10739680490503311
关键词
cytokines; endothelium; malaria; microcirculation; placenta; Plasmodium falciparum; platelet
资金
- NIAID NIH HHS [R01 AI34969] Funding Source: Medline
Severe malaria in humans and animals is initiated by interaction between malaria-infected cells, host blood Cells (including monocytes, T cells and platelets) and endothelial cells of the microcirculation. Adhesion to vascular cells, and possible vascular obstruction in severe human disease, involves interaction between host receptors and parasite-derived proteins, such as the variant antigen Plasmodium falciparum erythrocyte membrane protein 1 (PfEMP1). Our understanding of how different PfEMP1 variants may target infected erythrocytes to specific sites, such as the placenta, is rapidly increasing. However, in most instances downstream immune-mediated inflammatory processes appear more central than parasite accumulation to development of severe malaria. Using genetically-manipulated animal models of severe malaria, key roles for CD8 T cells and mediators such as lymphotoxin in the pathogenesis of murine disease have been established. Experimental and human studies suggest vascolar deposition of activated platelets may have a central role. Here, we review some recent advances in the understanding of severe malaria pathogenesis from human and animal studies, focusing on events at the level of microcirculation, and highlight the role for activated host cells in initiating the pathology of the disease.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据