and this post about it is from alt.support.skin-diseases.psoriasis ---
Hi,
Breaking news. We may be on the road to a potential cure. Ok
more like at the start of a path. LOL
DEATH RECEPTOR 3 ...Dr3
I'm down on death, unless we become really CLEAR and live
haPPily ever after.
Will Dr3 be a STAR or a NON starter?
http://www.sciencedaily.com/releases...0619120657.htm
Potential New Way To Block Inflammation In Autoimmune Disease
Discovered
ScienceDaily (Jun. 19, 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 Richard 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.
--
Nann
remove the Gator cheer to email me
Change everything. Love & forgive.
Potential New Way to Block Inflammation in Autoimmune disease 
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