Lupus Discovery May Hold Key to Better Treatment
Scripps Institute scientists have identified a series of specific cellular events that appear to be integral to the way lupus develops. The findings suggest that blocking this cellular pathway may be the secret to developing a truly effective way to battle the disease.
Systemic lupus erythematosus, or SLE, is an autoimmune disorder that affects tens of millions of people worldwide. More common in men than women, lupus affects the skin, joints, brains, kidneys and central nervous system, and other body organs and systems. Signs and symptoms of the disease include itchy and painful rashes, photosensitivity, severe joint and muscle pain, anemia, blood clots, kidney damage, fatigue, vision problems, hair loss, and extensive and widespread pain.
There are several current therapies for lupus, including steroids, immunosuppressant treatment, and anti-malarial drugs. But none of these treatments is able to zero in on the underlying causes of lupus, and all raise the patients’ risk of cancer and infections. The condition appears to arise from both genetic and environmental factors, and involves several complex autoimmune processes. The key feature in patients with lupus is the activity of antibodies that attack the body’s own nucleic acids and cellular proteins.
The research team from the Scripps Institute, led by Dr. Theofilopoulos, have long been at the forefront of lupus research. Recently, they’ve discovered evidence that a class of immune stimulating chemicals (known as type I interferons) are an essential function in the vicious lupus cycle. Certain immune cells will incorrectly identify self-proteins and nucleic acids as foreign, and will begin releasing the type I interferons. The interferons mobilize other elements of the immune system, including antibodies.
New evidence from the Scripps team suggests that the producers of those type I interferons in lupus patients are created by a fairly rare class of immune cells known as plasmacytoid dendritic cells. The discovery of the role of these pDCs’ will hopefully lead to the eventual development of a better course of treatment for lupus patients – one that stops the case of mistaken identity that starts the autoimmune cycle to begin with.