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Mechanism for generating autoimmunity-suppressing cells identified

PHILADELPHIA Autoimmune disorders, such as lupus, arthritis, and diabetes, are understood to result from immune cells attacking the bodys own cells instead of infectious agents such as viruses and bacteria. In a new study, scientists at The Wistar Institute have identified for the first time the mechanism by which the immune system generates regulatory T cells, a specialized type of immune cell that plays a critical role in preventing autoimmunity.

The findings suggest that regulatory T cells are finely tuned toward the recognition of the bodys own proteinsor selfand that a failure to make a complete repertoire of regulatory T cells may be an important factor in the development of autoimmune disease. In addition, the study suggests that engineering different types of regulatory T cells in the laboratory could one day become a strategy for combating autoimmune diseases.

The research is published in the April issue of Nature Immunology.

We and others showed previously that regulatory T cells suppress autoimmunity, but it was unknown how these cells were generated, says Andrew J. Caton, Ph.D., associate professor at The Wistar Institute and senior author on the study. Now, we believe we have good insight into that process.

Caton says the prevailing belief has been that the developing T cells most highly reactive to and specific for self proteins are eliminated by the body, and that developing T cells that are somewhat less specifically reactive to self are recruited for the regulatory function. Our findings contradict that notion and suggest that regulatory T cells recognize self proteins by a highly specific process, he says.

Research published last year by the same laboratory reported that as many as 10 percent of T cells in a normal animal are regulatory T cells, indicating their importance as a safeguard against autoimmunity.

Whats interesting about these regulato
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Contact: Marion Wyce/Franklin Hoke
wyce@wistar.upenn.edu
215-898-3943/3716
The Wistar Institute
27-Mar-2001


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