A :Potential New way to block inflammation in autoimmune disease

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I love this article fo I have an autoimmune disease. will ask my

Neuro-endocrine Dr about it. Sunds promising too enjoy heidi

Potential New Way To Block Inflammation In Autoimmune Disease

Discovered

ScienceDaily (June 24, 2008) — Researchers from the National

Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS),

a part of the National Institutes of Health (NIH), have identified a

promising new target for autoimmune disease treatment -- a cell-

surface receptor called DR3. Their research in mice suggests that

blocking this receptor could slow or stop the damaging inflammation

characteristic of autoimmune diseases, potentially without leaving

the body vulnerable to serious infections, as many current therapies

do.

DR3 is a protein on the surface of cells. It is a member of the tumor

necrosis factor (TNF) family of receptors, which bind to molecules

related to TNF, a cell-signaling protein that promotes inflammation.

Many of today's most potent treatments for inflammatory diseases,

such as rheumatoid arthritis and psoriasis, interfere with the action

of TNF, thereby blocking inflammation. Since current anti-TNF

therapies don't work in all autoimmune diseases, however, the

researchers turned to the study of DR3, which is a close relative of

TNFR1, the main receptor for TNF.

Working with mouse models of asthma and multiple sclerosis, both

immune system diseases, the researchers found that mice engineered to

lack DR3 were resistant to those diseases. " The implication is that

blocking DR3 in mice, and possibly in humans, is a potential therapy

for these diseases and perhaps others in which the immune system goes

awry, " said Siegel, M.D., Ph.D., a scientist in the NIAMS'

Immunoregulation Group, who led the research effort.

While closely related to TNFR1, DR3 is expressed in T cells, a

different kind of immune cell (a white blood cell that identifies and

fights infection) than those that express TNFR1, Dr. Siegel said. The

NIAMS group collaborated with a laboratory in Cardiff, Wales, which

had generated genetically engineered mice deficient in DR3, as well

as with a research group at the NIH's National Institute of Allergy

and Infectious Diseases (NIAID), which has developed mouse models of

disease with strong T cell components, such as asthma and multiple

sclerosis. " These findings open up new avenues for therapy of these

two diseases as well as to other autoimmune diseases in which T cells

play a role in causing or perpetuating the disease, " said Siegel.

The researchers hope that DR3-blocking agents will be effective anti-

inflammatory treatments someday. Siegel noted that if they were to be

used in rheumatic diseases, they would be a complement to strategies

that block TNF because they hit a different arm of the immune

system. " It could be potentially synergistic or complementary, " he

said.

Of critical importance, the NIAMS scientists found that removing DR3

did not appear to suppress the immune response or the ability to

fight infection within the mice -- a problem with many other

treatments for autoimmune disease. " We could see the effect of DR3

deficiency in the diseased organ, but when we looked systemically at

the immune response at other places in the mouse, it was barely

affected, " said Dr. Siegel.

The group's findings suggest that DR3-blocking agents might be more

effective at specifically treating autoimmune disease without

breaking down the body's defenses against infections, a long-sought

goal of researchers in the field