London, June 29 (ANI): Scientists at Imperial College London say that blocking a signal molecule made by the human body, which triggers the immune system into action, may make it possible to develop more effective treatments for rheumatoid arthritis.
Rheumatoid arthritis is the most common autoimmune disease that causes painful and persistent swelling in the joints, which can result in damage to the bone and cartilage.
Considering that around half of all patients do not respond to one or more of the treatments currently available, the researchers say that stopping the disease closer to the root of the problem could be the best way to treat it.
In their study paper, the researchers point out that the body responds to an infection by a microbe by turning on a molecular switch to set the immune system into action.
They say that their findings show that a signal molecule called tenascin-C can trigger the same molecular switch, and also activate the immune system.
They add that high levels of tenascin-C present in joints, therefore, may cause the activated immune system to attack the joint leading to the persistent inflammation of rheumatoid arthritis.
The researchers also reveal that the molecular switch called TLR4 is found on the surface of immune cells.
According to them, studies conducted in the past have shown that mice without TLR4 do not show chronic joint inflammation.
The team hope that scientists can develop new treatments that target the interaction between tenascin-C and TLR4, which may help to combat rheumatoid arthritis.
"Rheumatoid arthritis is a debilitating and painful disease and, unfortunately, there is no cure. Furthermore, current treatments are not effective for many patients," Nature magazine quoted Dr. Kim Midwood, lead author of the study from the Kennedy Institute of Rheumatology at Imperial College London, as saying.
"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," added Dr. Midwood.
The authors say that the next step will be to work out the precise mechanism by which tenascin-C increases these levels of inflammatory molecules in the human joint, and to find ways to inhibit this action.
A research article on their findings has been published in the journal Nature Medicine. (ANI)