New onset of chronic inflammation in rheumatoid arthritis found

A signal molecule in the human body, the immune system in action can play an important role in rheumatoid arthritis, new research published yesterday in Nature Medicine. The study, from Imperial College London, said that if scientists block that signal, it can be more efficient development of treatments for arthritis.

Rheumatoid arthritis is the most common autoimmune disease, which cover about 1 100 people. It creates painful and persistent in the joints, swelling, that may cause damage to bone and cartilage. About half of patients do not respond to one or more of the treatments currently available, and these may change over time less successful. The researchers behind the study say stop the disease close to the root of the problem would be the best way to treat and the results show, a new target for therapies.

If a microbe that infects the body, the body responds by clicking on a molecular switch for the immune system into action and protect the body against disease. Today, the results show that a signaling molecule called Tenascin-C may be at the same molecular switch and activate the immune system. High Tenascin-C in the joints can lead to the immune system, the common policy of the persistence of the inflammation of rheumatoid arthritis.

Molecular switches is TLR4 and lies on the surface of immune cells. Historical studies have shown that mice without TLR4 in fact, chronic inflammation of the joints. Researchers hope, scientists develop new therapies, the interaction between Tenascin-C and TLR4, the fight against rheumatoid arthritis.

Dr. Kim Midwood, lead-author of the study of the Kennedy Institute of Rheumatology at Imperial College London, said: "Rheumatoid arthritis is a painful disease and get worse and unfortunately, it ' there is no treatment. In addition, current treatments are not effective for many patients. "

"We have discovered a way that the immune system may be, for the joints in patients with rheumatoid arthritis. We hope that our new knowledge can help develop new therapies, Tenascin-C-activation of the immune system and the pain, inflammation, a hallmark of this condition, "adds Dr. Midwood.

The researchers reached their conclusions by five studies. One study suggested that Tenascin-C was required for ignition. The researchers induced in mice, inflammation of joints, with or without the gene for Tenascin-C. They found that mice can Tenascin-C has had severe joint swelling of the bone and cartilage destruction, but mice that do not Tenascin-C was no swelling and tissue destruction.

In a subsequent study, researchers injected the active Tenascin-C molecule in mice joints. They found one of the joints of the mouse to turn, and that this reaction has been intense with higher doses.

Another experiment showed that Tenascin-C causes swelling of the joints, the increase of the molecules that cause an inflammatory reaction. The researchers targeted immune cells and human macrophage cells, fibroblasts swollen articulation of patients with rheumatoid arthritis and added Tenascin-C. As a result of the Tenascin-C was added, the cells of molecules, an inflammation of the allergic reaction.

The authors plan to the exact mechanism by which Tenascin-C increases of these levels of inflammatory molecules in people and try to find ways for common action to prevent