Cytokines and thrombosis.

Cytokines are pleiotropic mediators of inflammation and immunity. Leukocytes and vascular cells are both sources of cytokines and targets for them. Several cytokines affect key functions of vascular wall cells. Several clinical acute or chronic inflammatory situations associate modifications of the cytokine network and a prothrombotic state. Many experimental data support the hypothesis that endothelial cells have an active role in these situations. Endothelial cells activated by cytokines such as tumor necrosis factor and interleukin-1 have decreased antithrombotic or prothrombotic properties and express leukocyte adhesion molecules to a greater extent. Cytokines, chemokines, and colony stimulating factors modulate the recruitment and activation of leukocytes. Activated platelets aggregate and bind to endothelial cells and to immobilized leukocytes, thus causing vascular occlusion accompanied by coagulation and leading to thrombosis. Cytokine activation may be limited by natural inhibitors or by therapeutic agents such as monoclonal antibodies, recombinant proteins, and drugs that alter cytokine synthesis, which may be of benefit in infection, inflammation, and possibly atherosclerosis.