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(Stroke. 2003;34:1417.)
© 2003 American Heart Association, Inc.

Original Contributions

Editorial Comment: Stroke and the CD40-CD40 Ligand System: At the Hinge Between Inflammation and Thrombosis

Neurologische Klinik, Städtisches Klinikum Ludwigshafen am Rhein, Ludwigshafen, Germany
Neurology Department, University of Heidelberg, Heidelberg, Germany

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Mounting evidence indicates that procoagulant and inflammatory pathways intertwine in complex networks and that inflammation contributes in an important way to atherogenesis and arterial thrombosis, ultimately leading to diseases such as ischemic stroke. Among the most intriguing recent findings was the detection of an important role of the potent immune mediator CD40 and its counterpart CD40 ligand (CD 154) in thrombosis and atherosclerosis. Initially thought of as solely mediating T lymphocyte–B lymphocyte interactions, CD40 was later also detected on monocytes/macrophages, smooth muscle cells, and endothelial cells. CD40 is an important activation receptor, whose engagement via CD40L endows these cells with powerful functions including the release of proinflammatory cytokines, adhesion receptors, tissue factor, metalloproteinases, and prostaglandins. CD40L, a transmembrane protein structurally related to tumor necrosis factor-, was initially identified on T lymphocytes. Surprisingly, it was later also detected on platelets. CD40L is rapidly upregulated during platelet activation and triggers an inflammatory response in cells that constitutively express CD40 such as endothelial cells and monocytes/macrophages.¹ Thereby activated platelets generate signals for the recruitment of leukocytes to the site of injury and thrombogenesis and can rapidly incite a cascade of inflammation by interacting with cells of the vasculature.

The scenario is more complex as CD40-bearing cells such as endothelial cells, smooth muscle cells, and macrophages also store CD40L that may be used to amplify cell stimulation in an autocrine way.² And platelets also constitutively express CD40. The binding of CD40L to coexpressed CD40 in a platelet aggregate leads to cleavage of CD40L, . . . [Full Text of this Article]

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