ls that had similar clinical signs, the researchers
hypothesized the animals were producing too much of a potent inflammatory
protein called tumor necrosis factor alpha (TNFa).
To test their idea, the researchers injected the TTP-deficient animals
with an antibody that neutralizes TNFa. In a dramatic and almost complete
reversal, all signs of disease completely disappeared.
The findings support preliminary results of human clinical trials being
conducted at Duke and other research institutions of an experimental treatment
for rheumatoid arthritis (RA) that also uses antibodies to TNFa, Blackshear
said. Such studies have shown antibodies to TNFa can significantly reduce
the symptoms of RA in patients.
"We know that TNFa is involved in many human inflammatory diseases
including autoimmune disorders and septic shock," Blackshear said.
"This finding provides insight into a new gene that appears to regulate
TNFa. It is possible that defects in this gene may cause people to be susceptible
to developing autoimmune diseases."
The corresponding gene has been identified in people, and Blackshear's
group will soon begin a study to see if mutations in the gene correlate
with autoimmune disease in people.
"The TTP-deficient mouse is an exciting new model of arthritis,"
said Haynes, chairman of medicine at Duke and director of the Duke University
Arthritis Center. "It also provides important new information about
the types of genes that can cause arthritis."
In addition to using the animal model to understand the autoimmune response,
Blackshear will continue studies to determine how TTP is involved in the
"Right now we really don't have a good handle on what TTP is doing,
although there are hints it is involved in gene regulation," Blackshear
said. "Our next step will be to determine if it is involved in synthesis
or degradation of TNF_ and then move forward to our original question of
how TTP i
Contact: Karyn Hede George
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