期刊
MOLECULAR IMMUNOLOGY
卷 47, 期 13, 页码 2170-2175出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.molimm.2010.05.009
关键词
Platelets; Complement; Thrombosis; Inflammation; Systemic lupus erythematosus; Antiphospholipid syndrome; Immune thrombocytopenia purpura
资金
- NHLBI NIH HHS [R01 HL067211, HL67211, R01 HL067211-04] Funding Source: Medline
- NIAID NIH HHS [AI060866, R56 AI060866, R01 AI060866] Funding Source: Medline
Platelets participate in a variety of responses of the blood to injury. An emerging body of evidence suggests that these cells express an intrinsic capacity to interact with and trigger both classical and alternative pathways of complement. This activity requires cell activation with biochemical agonists and/or shear stress, and is associated with the expression of P-selectin, gC1qR, and chondroitin sulfate. Platelet mediated complement activation measurably increases soluble inflammatory mediators (C3a and C5a). Platelets may also serve as targets of classical complement activation in autoimmune conditions such as antiphospholipid syndromes (APS) and immune thrombocytopenia purpura (ITP). Retrospective correlation with clinical data suggests that enhanced platelet associated complement activation correlates with increased arterial thrombotic events in patients with lupus erythematosus and APS, and evidence of enhanced platelet clearance from the circulation in patients with ITP. Taken together, these data support a role for platelet mediated complement activation in vascular inflammation and thrombosis. (C) 2010 Elsevier Ltd. All rights reserved.
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