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A new hypothesis about autoimmunity. Is it possible to be too clean?

La Jolla, CA. April 12, 2004 - A group of scientists at The Scripps Research Institute have found a connection between poor T cell survival in the body and the development of autoimmunity.

On the basis of this connection, the scientists are proposing a new hypothesis about the cause of autoimmunity, in which components of a person's immune system attack his/her own tissues leading to diseases such as Type 1 diabetes and rheumatoid arthritis.

"Autoimmunity has [traditionally] been considered a condition of too much stimulation," says Scripps Research Immunology Professor Nora Sarvetnick, Ph.D. "What we are seeing is that it is a condition of too little stimulation."

In an article appearing in this week's issue of the journal Cell, Nora Sarvetnick and her coauthors in the Department of Immunology assert that we need a certain level of immune stimulation to fill the body with immune cells. An understimulated immune system results in too few T cells, and the body tries to correct this by inducing a vigorous expansion of the remaining T cells, creating a more autoreactive population.

The hypothesis explains why childhood bacterial infections decrease the risk for developing autoimmune diseases and explains why autoimmunity has been rising in the last half century in populations with decreased exposure to pathogens.

It also provides a new way for thinking about how to make autoimmune diseases more preventable. The key to decreasing the chances of developing autoimmunity may be to stimulate the immune system by priming people with germs.

Autoimmunity and Lymphopenia

Autoimmune diseases are to biology as friendly fire is to war.

Normally, the body's immune system is designed to recognize invading viruses or bacteria and destroy them. But in autoimmune diseases, the body's response is not limited to pathogens. Instead, the body manufactures cells and molecules that attack its own tissues and organs.
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Contact: Jason S. Bardi
jasonb@scripps.edu
858-784-9254
Scripps Research Institute
15-Apr-2004


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