Researchers at Imperial College London published a study in which they found that blocking an immune system trigger molecule made by the human body may lead to development of more effective treatments for rheumatoid arthritis (RA).
In their research paper, the scientists state that the body responds to an infection by turning on a molecular switch which puts the immune system into action.
What they found was that a signal molecule called tenascin-C can trigger the same molecular switch, and that tenascin-C can also activate the immune system.
In addition, they theorize that elevated levels of tenascin-C present in joints may cause the activated immune system to attack the joint which could lead to rheumatoid arthritis.
The researchers also reported that they found another molecular switch, called TLR4, on the surface of immune cells. Previous studies have shown that mice without TLR4 do not have chronic joint inflammation.
Lead author, Dr. Kim Midwood from the Kennedy Institute of Rheumatology at Imperial College London, said: “Rheumatoid arthritis is a debilitating and painful disease and, unfortunately, there is no cure. Furthermore, current treatments are not effective for many patients.”
“We have uncovered one way that the immune system may be triggered to attack the joints in patients with rheumatoid arthritis. We hope our new findings can be used to develop new therapies that interfere with tenascin-C activation of the immune system and that these will reduce the painful inflammation that is a hallmark of this condition,” add Dr. Midwood.
The authors say that the next step will be to work out exactly how tenascin-C increases the level of inflammatory molecules in the human joint, and to find ways to inhibit this action.
The team’s research was been published in the journal Nature Medicine.
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Originally posted 2009-07-01 14:43:25. Republished by Blog Post Promoter
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