RSR’s main research activities are centred on investigating various autoimmune diseases. In these conditions, the body’s immune system attacks some of the body’s own tissues rather than limiting its action to attacking invading pathogens such as bacteria and viruses. This process of "self attack" is known as autoimmunity and different tissues are affected in different diseases. For example in the diabetes of childhood (type 1 diabetes mellitus) the immune system attacks and destroys the insulin producing cells of the pancreas. In Graves’ disease the thyroid gland is attacked in such a way as to cause the gland to be overactive. In Addison’s disease, the steroid producing cells of the adrenal gland are attacked and destroyed by the immune system. The muscle weakness characteristic of myasthenia gravis is due to the immune system attacking the junction between nerves and muscles (the neuromuscular junction).

Currently, about 15 different major autoimmune diseases are recognized and altogether they affect about 3% of the population. The reason why autoimmunity develops is still not known but better progress is being made in understanding the mechanisms by which the immune system causes its effects. In particular, the immune system has 2 principle modes of attack – a cellular mode in which the target organ is attacked by immune cells and a humoral mode in which the target organ is attacked by protein molecules called antibodies. Usually both immune cells and antibodies are involved in autoimmune diseases. Antibodies (or autoantibodies in the case of antibodies which attack the body’s own tissues) are much easier to study and measure than immune cells.

Autoantibodies bind to (i.e. recognise) specific molecules in the tissues which are under autoimmune attack. These molecules are known as autoantigens. For example, in the case of myasthenia gravis, autoantibodies bind to the receptor for acetylcholine in the neuromuscular junction. In the case of Graves’ disease, autoantibodies bind to the receptor for thyroid stimulating hormone on the surface of thyroid cells. In Addison’s disease, autoantibodies bind to a key enzyme in the adrenal gland (21-hydroxylase) involved in steroid synthesis. In type 1 diabetes, autoantibodies recognise insulin, an enzyme called glutamic acid decarboxylase, a protein called IA-2 and zinc transporter 8 (ZnT8). In the case of Neuromyelitis Optica (NMO), autoantibodies bind to a water-channel protein aquaporin 4 (AQP4).

Understanding the details of autoantigen – autoantibody interactions at the molecular level is an important goal of RSR’s research programme as is identifying new autoantigens and autoantibodies. This programme should lead to better ways of diagnosing and managing patients with autoimmune disorders.

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