Systemic Lupus Erythematosus is one of the classic examples of autoimmune diseases among human beings. Clinically it is an unpredictable remitting, relapsing disease of acute onset that may involve virtually any organ in the body; however it principally effects the skin, kidney, serosal membranes, joints and heart. There are no strict symptoms of SLE however weakness, fatigue, weight loss, pain headache and skin rash are few of the very commonly observed symptoms (Price et al, 2002).In last couple of years many scientists have shown keen interest in exploring the disease to the depths of molecular level. Three important areas of their studies are: 1- Role of gender in acquiring Systemic Lupus Erythematosus. 2- Autoantibodies associated with the disease. 3- Role of certain lymphokines and T cells in the development and acquiring of disease. .
It was long ago observed that Systemic Lupus was far more common in females than males, approximately with a ratio of 9:1(Rider et al, 1998). Several theories were proposed to explain the existence of the phenomenon. The explanation that gained most popularity and acceptance was the one give by Dr. Rider with the team at University of Missouri-Kansas. Dr. Rider proposed hormonal influence in the having and carrying of disease (Rider et al, 1998). Twelve SLE patients were tested against nine normal female patients. Blood samples were obtained at certain interval of time from both the normal and the diseased individuals, T cell population obtained were very carefully analyzed and observed. The obtained samples were clinically analyzed through series of tests. And it was shown that estrogen was the key factor. This experiment presented the early idea of a mechanism by which estrogen plays a role in gender difference in a disease like Systemic Lupus Erythomatsus. The data and observations obtained from the experiment suggest that Estrogen increases the expression of intracellular calcineurin in patients suffering from SLE evident by increased sensitivity of the T cell population obtained from the diseased individual, where as the T cell population obtained from the normal individuals did not exhibited any such sensitivity.