According to new research published June 28, 2009 in Nature Medicine, scientists have uncovered one molecular switch that triggers the immune system to attack the joints in people with rheumatoid arthritis.   The authors of the study from Imperial College London state that blocking this signal may provide effective arthritis treatments in the future. Approximately 1 percent of the population suffers from rheumatoid arthritis the most common autoimmune disease.  About half of all patients are not responding to the current treatments available today.  Research scientists working on this study state that stopping this disease closer to the root of the problem could possibly be the best way to treat the disease.  The results from their study suggest a new direction for therapies.

In healthy people when a microbe invades the body the immune system responds by turning on a molecular switch that sends the immune system into action to protect the body from disease.  In this study, the signal molecule called tenascin-C can trigger the same molecular switch and activate the immune system.  High levels of this signal molecule tenascin-C in joints may cause the activated immune system to attack the joint tissue that leads to persistent inflammation that is common in rheumatoid arthritis.  The molecular switch is called TLR4.  It is found on the surface of the immune cell and in prior research mice without TLR4 do not show chronic joint inflammation.

The researchers in this study are hopeful that scientists can develop new treatments that target the interaction between tenascin-C ( the signal molecule ) and TLR4( the molecular switch ). This may help to combat rheumatoid arthritis.  Dr. Kim Midwood, the head author of this study from the Kennedy Institute of Rheumatology at Imperial College in London states that “We have uncovered on 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.”

The researchers conducted 5 studies.  One study suggests that tenascin-C is needed to sustain inflammation.  They produced joint inflammation in mice with and without the gene for tenascin-C and found that the mice without the gene for tenacin-C showed no swelling or tissue distructions however the mice with the gene that could produce tenascin-c had severe swelling in the joint and bone and cartilage damage.  In a later study, mice joints were injected with the active part of the tenacin-C molecule. Researchers found that it caused the joints of the mice to become inflamed and with higher doses the reaction was more intense. In another study, scientist found that by taking human immune cells called macrophages and fibroglasts from the swollen joints of patients with rheumatoid arthritis and adding tenascin-C the cells produced more molecules that cause inflammation.The study authors are planning on working out the exact mechanism in tenacin-C that increases these levels of inflammation in the joint and explore way to inhibit it.

Tags: arthritis, autoimmune, condition, diseasse, doses, Dr. Kim Midwood, fibroglasts, gene, immune, Imperial College London, Kennedy Institute of Rheumatology, microphage, Nature Medicine, painful, research, rheumatoid, system, tenacin-C, TLR4

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