Autoimmune disease comprises conditions that result from abnormal immune system function.  The characteristic feature is the development of antibodies that inappropriately identify certain aspects of the host (self) system as foreign or abnormal.  These are termed auto-antibodies.

The immune system normally produces antibodies in response to invading organisms and unregulated abnormal (cancerous) cells.  Regulatory mechanisms exist that aim to prevent an excessive immune system response to these antigens (foreign particles) as well as avoiding an inappropriate attack against normal (self) tissue.  An example of this is the destruction of certain immune cells, called T cells, which demonstrate the capacity to react against self within the Thymus gland early in life.

Why these auto-antibodies develop has yet to be completely explained.  A popular theory is that the immune system encounters a foreign organism, such as a virus, triggering an appropriate response to fight the infection.  However, the part of the organism that is seen as abnormal, termed the antigen, looks very similar to a part of normal cells within the host.  As a result the immune system continues its response against the target it has identified wrongly within the host system, causing the autoimmune disease. 

Unfortunately, this theory in isolation is too simple and does not explain the entire story.  There are, in addition, many other factors that impact upon the development of autoimmune disorders.  These include genetic factors, either individual genes or the balance of many, as well as the hormonal milieu.  Understanding the role of these factors remains a major focus of ongoing research, which is ever increasing with respect to genetics.  The importance of hormones is highlighted by the fact that autoimmune disorders are generally much more common in women.

Therefore, a more accurate hypothesis is that an autoimmune disorder occurs in a genetically predisposed host, at a time during which the hormonal milieu is supportive, when exposed to an environmental antigen that mimics normal tissue thereby triggering an inappropriate immune response.

The clinical manifestation of the specific autoimmune disease is determined by the specific auto-antibodies present and the sites at which the auto-antigens are expressed.  The variation in these factors is what is responsible for the large number of autoimmune disorders that exist.  This explains why an autoimmune disease may affect a single organ, such as occurs in Hashimotos’ thyroiditis, or many different organs such as in the classical autoimmune disease Systemic Lupus Erythematosus (SLE). 

The cornerstone of treatment, in most cases, is the suppression of the immune system.  The traditional options include Prednisone, Cyclophosphamide, Azathioprine, amongst many others.  These medications are non-specific in their actions, meaning that they suppress many different parts of the immune system including those which play no part in the pathogenesis of the particular disease.  The consequence is that there is an increased risk of complications, especially including infections and malignancy.  As a result, devising a method to specifically manipulate and suppress the immune system in a targeted manner is the subject of a large body of current research.  It is in this area that major advances in these disorders are likely to eventuate.