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Study identifies novel role for a protein that could lead to new treatments for rheumatoid arthritis
Date:5/22/2011

A new study by rheumatologists at Hospital for Special Surgery in New York has shown that a powerful pro-inflammatory protein, tumor necrosis factor (TNF), can also suppress aspects of inflammation. The researchers say the identification of the mechanism of how this occurs could potentially lead to new treatments for diseases such as rheumatoid arthritis. The study was published May 22 online in advance of publication in the journal Nature Immunology.

"Prior to this study, TNF has long been known as a potent pro-inflammatory cytokine, but if you look carefully through the literature, there are hints that it also has some suppressive functions, but nothing was known about the mechanisms," said Lionel Ivashkiv, M.D., associate chief scientific officer and physician in the Arthritis and Tissue Degeneration Program at Hospital for Special Surgery who led the study. "This is really the first mechanism showing how TNF can turn inflammation down."

Because many proteins have homeostatic functions, both driving and suppressing certain actions so a cell can maintain internal equilibrium, researchers thought TNF might not be an exception. "Most strong activators in the immune system trigger a feedback response to restrain the amount of inflammation," Dr. Ivashkiv said.

To find out, researchers designed experiments stimulating macrophages with lipopolysaccharide (LPS), a prototypical inflammatory factor that stimulates receptors important in inflammation. In test tube studies, the researchers treated human monocytes and macrophages, cells that have a key role in inflammatory diseases, with TNF and then challenged these cells with LPS. They found that the TNF suppressed the inflammatory response of the macrophages and monocytes. They then gave mice low doses of TNF followed by high doses of LPS and found that the mice were protected from the effects of high dose LPS, which is usually lethal. They discovered that the mechanism by which TNF
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Contact: Phyllis Fisher
phyllis.fisher@gmail.com
212-606-1197
Hospital for Special Surgery
Source:Eurekalert

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