Inflammation is a process by which the white blood cells and chemicals of the immune system rally to protect the body from infection and foreign substances such as bacteria and viruses. In autoimmune diseases, however, this defense system triggers an inflammatory response when there are no foreign substances to fight off, or the defense system goes into "overdrive" and forgets how to turn off. In these diseases, the body's normally protective immune system attacks and damages its own healthy tissues.
UCSD researcher Mark H. Ginsberg, M.D., professor of Medicine at the University of California, San Diego (UCSD) School of Medicine, and his colleagues have identified a mechanism to selectively disrupt signaling to recruit lymphocytes and monocytes white blood cells sent to sites of inflammation to fight infection while maintaining the body's other essential immune system functions. Their findings appear online on February 9 in advance of print publication in the March issue of the Journal of Clinical Investigation.
In the case of certain autoimmune diseases, the alpha 4 integrins cause white blood cells to accumulate at the site of the disease, resulting in inflammation. An integrin is a surface molecule found on the exterior of cells that helps cells adhere and migrate. It is also believed to be responsible for a role in cell signaling, which allows cells to communicate with the extracellular environment. One of the promising treatments for disorders such as multiple sclerosis, inflammatory bowel disease and rheumatoid arthritis the alpha 4 integrin antagonist works by blocking cell adhesion. However, this anti-inflammatory therapy could cause adverse side effects, such as impairme
Contact: Debra Kain
University of California - San Diego