期刊
AMERICAN JOURNAL OF TRANSPLANTATION
卷 9, 期 1, 页码 14-22出版社
WILEY
DOI: 10.1111/j.1600-6143.2008.02473.x
关键词
Chemokines; endothelial cells; ischemia; macrophage; platelet; rejection; T cell
资金
- Georgia Research Alliance
- McKelvey Foundation
- NIH [R01 AI42387, P01 HL70295, P01-HL56091, 5K08HL74945-5]
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [P01HL070295, P01HL056091, K08HL074945] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI042387] Funding Source: NIH RePORTER
This review relates the basic functions of platelets to specific aspects of organ allograft rejection. Platelet activation can occur in the donor or recipient before transplantation as well as during antibody- and cell-mediated rejection. Biopsies taken during organ procurement from cadaver donors have documented that activated platelets are attached to vascular endothelial cells or leukocytes. In addition, many patients waiting for transplants have activated platelets due to the diseases that lead to organ failure or as a result of interventions used to support patients before and during transplantation. The contribution of platelets to hyperacute rejection of both allografts and xenografts is well recognized. Intravascular aggregates of platelets can also be prominent in experimental and clinical transplants that undergo acute antibody or cell-mediated rejection. In acute rejection, platelets can recruit mononuclear cells by secretion of chemokines. After contact, monocytes, macrophages and T cells interact with platelets through receptor/ligand pairs, including P-selectin/PSGL-1 and CD40/CD154. There is a potential for therapy to inhibit platelet mediated immune stimulation, but it is counterbalanced by the need to maintain coagulation in the perioperative period.
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