Pathophysiology of lupus is currently being studied in all areas of the disease and many believe it could be a way to abolish the disease. Systemic lupus erythematosus (SLE) is an autoimmune disease in which the body’s immune system attacks its own healthy tissue. Pathophysiology is defined as the study the biological and physical manifestations of disease as the correlate with the underlying abnormalities and physiological disturbances. In other words, Pathophysiology of SLE looks at the specific malfunction (such as skin rashes) that comes from or causes disease.

One problem is that abnormal activity is not the same in each lupus patient. For example, many genes that affect the immune function may cause the susceptibility of clinical diseases such as lupus. However, this is not always so.  Some studies in identical twins do not correlate, which shows that additional factors, other than genetics, are involved in triggering the widespread development of autoimmunity in susceptible individuals. These factors are probably environmental, but this is still unknown.


Pathophysiology of Systemic Lupus Erythematosus


One big question in the pathophysiology of systemic lupus erythematosus (SLE) is why does one environmental factor produce lupus in one person and not in another? The explanations people have found in different lupus cases don’t always connect. For example, people who have been infected with the Epstein Barr virus have later been known to get lupus. However, not everyone who has had this virus later develops lupus. gives an explanation to the pathophysiology of Systemic Lupus Erythematosus (SLE). It states that the immune system must have a balance between being able to protect itself from infection, yet too sensitive to attack its own proteins.  Some genetic combinations result in autoimmunity. However, sometimes it takes some sort of environmental factor to trigger it, such as ultraviolet light, drugs, and viruses.

Researchers believe that by identifying the genes that produce certain proteins they can help to cure the disease. The idea is that each gene contains proteins, and each protein is a link on the autoimmune chain and if drugs can be created to break those links, the disease can be cured.

In a recent study of the pathophysiology of lupus erythematosus, a nuclear protein had been found to be present in patients and in mice with systemic lupus erythematosus. The protein is called high mobility group box 1 (HMGB1). It is increasingly evident that HMGB1 has properties which contribute to inflammation and autoimmunity. This may be a key connection that will someday help in developing drugs to abolish autoimmune diseases.