ICAM-1: Difference between revisions
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Latest revision as of 14:20, 17 March 2025
ICAM-1 (InterCellular Adhesion Molecule 1), also known as CD54 (Cluster of Differentiation 54), is a type of protein that is encoded by the ICAM1 gene in humans. ICAM-1 is a member of the immunoglobulin superfamily, and is a cell surface glycoprotein which is typically expressed on endothelial cells and cells of the immune system.
Function[edit]
ICAM-1 plays a crucial role in the immune response and inflammatory processes. It functions as a cell adhesion molecule, meaning it helps cells stick together. Specifically, ICAM-1 facilitates the adhesion of leukocytes (white blood cells) to the endothelial cells that line the blood vessels. This is a key step in the immune response, as it allows these immune cells to exit the bloodstream and enter the tissues where they can fight infection.
ICAM-1 also plays a role in lymphocyte activation, antigen presentation, and apoptosis (programmed cell death). It can bind to various integrins, including LFA-1 and Mac-1, which are found on the surface of leukocytes.
Clinical significance[edit]
Alterations in ICAM-1 expression have been associated with a variety of diseases. For example, increased levels of ICAM-1 have been observed in patients with autoimmune diseases such as rheumatoid arthritis and lupus. ICAM-1 is also involved in the pathogenesis of atherosclerosis, a disease characterized by the buildup of plaque in the arteries.
In addition, ICAM-1 has been implicated in the spread of certain viral infections. Some viruses, including the rhinovirus (common cold virus) and the malaria parasite, use ICAM-1 as a receptor to enter cells.
Research[edit]
Research into ICAM-1 has led to the development of several therapeutic strategies. For example, drugs that block ICAM-1 are being investigated for the treatment of inflammatory and autoimmune diseases. In addition, ICAM-1 has been explored as a potential target for cancer immunotherapy, due to its role in immune cell activation and migration.
See also[edit]

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