Cell adhesion molecules (CAM) expressed in vascular endothelium ensure integrity of the endothelial layer, recruitment and transmigration of leukocytes. Being receptors of many viruses, they play a role in immune control and infectious processes. Monoclonal anti-ICAM-1 antibodies enhance infection of primary human umbilical vein endothelial cell (HUVEC) cultures with HIV-1 due to incorporation into virions. IFN-gamma activates expression of ICAM-1 on HIV-infected HUVEC and thereby promotes binding of this molecule to complementary molecules on a greater number of sensitive cells, virion transfer onto them, and broad dissemination of the virus. Recombinant human IFN-alpha, IFN-beta and IFN-gamma influence (activate, inhibit) CAM shedding from HUVEC both intact and infected wit HSV-1. Activated shedding in the blood stream due to competition between soluble and endothelial CAM slows down recruitment and transmigration of leukocytes, i.e. regulates inflammation. CAM incorporated in microparticles can influence a wide spectrum of pathological processes Endothelial CAM may be a target for the delivery of pharmaceuticals for the treatment of vascular (including infectious) pathology.

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