In genetically predisposed, at-risk subjects environmental stressors trigger changes in self antigens in the mucosal layer in the joints. This in turn evokes a pathological immune response both cellular and humoral. Often it takes years before it manifests as clinical disease. Over time the inflammation localised at the joint synovia destroys the cartilage and damages the bone. Quality of life is severely reduced. It is important to note that RA does not exclusively involve the joints. Premature deaths are often linked to RA-associated interstitial lung disease and cardiovascular failure.

The diagnosis of RA and assessment of its severity are based on the American College of Rheumatology/ European League Against Rheumatism Collaborative Initiative, known as the ACR/EULAR criteria. This once severely debilitating disorder is now more manageable, but no curative treatment is available. Treatment regimens are cumbersome and have limited effectiveness. Disease-modifying antirheumatic drugs (DMARDs) are a combination of several immunosuppressive medications (Methotrexate, Sulfasalazine, Azathioprine etc.) often combined with anti-inflammatory agents such as steroids. Even with aggressive DMARD regimes started early in the disease process, remission is achieved in less than 25% of cases.

There is a clear need for a radical novel approach: new therapeutic modality to arrest the autoimmune destruction.

The Technology:

Our Antigenic Immune Modulatory (AIM) platform utilises the commonality between different autoimmune diseases. All are characterised by loss of self-tolerance to self-antigen with an appreciable symptom-free preclinical period. Thus, our AIM platform is designed to be therapeutic as well as preventive.

The difference between autoimmune diseases is fundamentally with regard the autoantigen. Thus, a unified, autoantigen-based, AIM approach has great potential to succeed across differing autoimmune diseases.