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Chemical Messenger Inactivates Cellular "Police" in Multiple Sclerosis

For release: Friday, October 28, 2005

One of the fundamental mysteries of autoimmune diseases is how normally protective immune responses go bad.  A new study sheds some light on this issue by showing that a chemical messenger called interleukin 12, or IL-12, allows some white blood cells to proliferate and damage healthy tissues.  This finding may lead to new drug treatments for multiple sclerosis (MS) and other autoimmune diseases.

In MS and other autoimmune diseases, certain cells of the immune system -- designed to search out and attack disease-causing viruses and bacteria -- instead attack healthy tissue in the body.  White blood cells called effector T cells are a part of the body’s natural defense system and trigger an inflammatory response to fight off foreign substances.  Other white blood cells, called T-regulatory cells, “police” the effector T cells to limit inflammation. “Normally, effector T-cells are under strict control as they circulate through the bloodstream in order to prevent unnecessary inflammation that could be harmful to  healthy tissues,” says Benjamin Segal, M.D., the neurologist who led the study at the University of Rochester in New York. “However, occasionally, they escape the body’s suppression system. We’re learning how they do that.” The new study on the cause of this autoimmune attack, was funded in part by the National Institute of Neurological Disorders and Stroke (NINDS), a component of the National Institutes of Health (NIH), and appeared in the July 15, 2005, issue of the Journal of Immunology*.

Dr. Segal’s research began in Dr. Ethan Shevach’s intramural laboratory at the NIH, where he was one of the first scientists to demonstrate that IL-12 played an important role in autoimmune diseases like MS.  In studies in the 1990’s, Segal and Shevach showed that mice without the IL-12 gene are completely protected against a disease similar to MS. In contrast, exposing normally harmless effector T cells to IL-12 appears to trigger an MS-like disease state. 

Dr. Segal and colleagues have shown that the chemical messenger IL-12 inactivates T-regulatory cells, allowing “renegade” effector T cells to circulate in the central nervous system.  The new study may explain why people with MS are more likely to suffer a relapse of the disease when they get an infection like the flu.  When a person is infected, IL-12 levels rise to allow the person to fight off the infection.  This flu-induced IL-12 increase may lead to a relapse by promoting autoimmune effector T cells.  These autoimmune T cells are believed to mediate damage to myelin, the fatty covering that wraps around and protects nerve fibers.  The researchers hope that understanding this chain of events will lead to the development of better treatments for MS and other autoimmune diseases.

An experimental drug that inhibits IL-12 is currently being tested by Dr. Segal and others as treatment for patients with relapsing-remitting MS, the most common form of the disease.  The scientists believe that IL-12 inhibition could also be useful in other autoimmune diseases such as Crohn’s disease, psoriasis, and rheumatoid arthritis. 

The NINDS is a component of the National Institutes of Health within the Department of Health and Human Services and is the nation’s primary supporter of biomedical research on the brain and nervous system.  The National Institutes of Health (NIH) is comprised of 27 Institutes and Centers and is a component of the U. S. Department of Health and Human Services.  It is the primary Federal agency for conducting and supporting basic, clinical, and translational medical research, and investigates the causes, treatments, and cures for both common and rare diseases.  For more information about NIH and its programs, visit

*King, IL and Segal, BM. “Cutting Edge: IL-12 induces CD4+CD25-T cell activation in the presence of T regulatory cells.” The Journal of Immunology, July 15, 2005, Vol.175, pp.641-645.

-By Michelle D. Jones-London, Ph.D.

Last Modified January 31, 2007