Discovering exactly what causes rheumatoid arthritis has long tested the best scientific minds and while science is no nearer revealing exactly how and why the body’s immune system turns on itself, research so far has revealed one specific defence against the condition – the presence of a specific variety of white blood cells known as regulatory T cells, or Tregs.
The right combination of Tregs is required to control or boost the immune system’s inflammatory response. This is an important factor in rheumatoid arthritis because it is an autoimmune disease where the immune system attacks the joints, causing inflammation.
The diversity of the Tregs present in the body, when activated as molecules called T cell receptors, can stop the immune system attacking the tissue in the joints and producing the inflammation that is the main feature of rheumatoid arthritis. The T cell receptors are essential for helping the immune system to identify which molecules are “friendly” or “self” – ie foe.
New research carried at the Wistar Institute, and reported in the Journal of Immunology, tested if T cell receptors could suppress arthritis in a mouse bred with the arthritis “self” and concluded that only a variety of Tregs could actually stop arthritis from developing as, working together, they have a positive influence on other parts of the immune system.
The Tregs considered specific for targeting the “self” molecule to suppress the immune response was not as effective on its own with the research team concluding that several inflammation-stimulating antigens and not simply one may be the cause of the condition.
Identifying which parts of the immune system are involved in developing rheumatoid arthritis has important consequences for potential new treatments for the condition. Research is also focusing on why rheumatoid arthritis specifically targets the membrane surrounding the joints with one theory positing that the flawed cells naturally gather in those parts of the body because of the Tregs’ influence.
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