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Autoimmune Disease Treatment May Not Dampen Immune System
Date:6/19/2008

Targeting a key protein might reap rewards for people with asthma, MS, scientists say

THURSDAY, June 19 (HealthDay News) -- Researchers have uncovered cellular proteins that may be key to certain autoimmune and inflammatory diseases, according to a new study.

The findings, performed so far only in mice, point to potential new treatments for a range of human diseases that are mediated by immune system T-cells. These include many inflammatory and autoimmune disorders, illnesses that involve an immune system run amok.

More important, such a treatment might provide patients with all the benefits of existing drugs, without the general immune suppression that often accompanies them.

"It has an effect on an autoimmune disease -- a mouse model of multiple sclerosis -- and an inflammatory disease -- a mouse model of asthma -- but does not seem to interfere with protective immunity against toxoplasma, a parasite," said one expert, Dr. Noel Rose, director of the Johns Hopkins Center for Autoimmune Disease Research in Baltimore.

"This is what everyone is driving for, to selectively block pathological [immune] responses but not normal responses," added the study's lead author, Dr. Richard Siegel of the U.S. National Institute of Arthritis and Musculoskeletal and Skin Diseases.

The findings were published in the July issue of Immunity.

At the center of this effort are a pair of proteins, DR3 and TL1A. Expressed on the surface of white blood cells called T lymphocytes, DR3 induces T-cells to proliferate and release inflammatory cytokines (signaling proteins) when it binds TL1A, which is like the "key" to DR3's "lock."

TL1A and DR3 are also related to tumor necrosis factor (TNF), and its receptor, respectively. TNF has been implicated in inflammatory and autoimmune disease, and drugs that target TNF and its receptor are used to treat rheumatoid arthritis and inflammatory bowel
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