Systemic Lupus Erythematosus (SLE or Lupus) is a systemic autoimmune disease that affects many joints and organs in the body. In lupus, like rheumatoid arthritis (RA), the patient’s immune system attacks their own healthy tissues. Lupus research funded by the Arthritis National Research Foundation is focused on understanding systemic lupus so we can find new treatments and a cure.
Initially, in Systemic Lupus Erythematosus, the tissues being attacked are different from RA, however, in later stages, the diseases become very similar. ANRF funded research on the pathology and causes of lupus is revealing new approaches towards developing therapies and a cure.
The Arthritis National Research Foundation has funded research on lupus for over 30 years, including renowned researchers like Betty Tsao, PhD, a leading geneticist at UCLA. Dr. Tsao is the first scientist to tie a specific human chromosome region to increased risk of developing Systemic Lupus Erythematosus. This is a major step for lupus research towards predicting susceptibility to lupus and understanding how to prevent the onset of symptoms.
Staying committed to funding autoimmune arthritis research, such as lupus research, is important to everyone at ANRF. The next big discovery, treatment, therapy or cure could be in the next research project. Read below about some of the exciting lupus research happening around the country.
Hong Zan, PhD
University of Texas Health Science Center
San Antonio, TX
Dr. Zan is developing new therapies targeting estrogen and other factors that dampen the autoimmune response in lupus.
Systemic lupus erythematosus (SLE or lupus) is an autoimmune disease in which the immune system turns against parts of the body it is designed to protect. With lupus, instead of producing protective antibodies, the immune system makes autoantibodies, which attack the patient’s own tissues and cause widespread tissue and organ injury.
The pathogenesis of autoimmune diseases, including lupus, can be traced to both genetic elements and epigenetic modifications arising from exposure to the environment. Epigenetics involves genetic control by factors other than an individual’s own DNA sequence. These epigenetic factors can switch genes on or off. Like many other autoimmune diseases, lupus preferentially affects women during their reproductive years, suggesting that the female hormone, estrogen, plays an important role in causing lupus.
Potential: Dr. Zan utilizes FDA-approved and widely-used epigenetic modulators to selectively inhibit the generation of disease-causing autoantibodies to prevent, treat or even cure lupus. With the second year support from Arthritis National Research Foundation, he will develop therapeutic approaches to dampen autoantibody responses and thereby treat lupus more effectively.
J. Michelle Kahlenberg, MD, PhD
University of California, San Francisco
Dr. Kahlenberg is working to demonstrate the causal connection between skin injury and kidney disease in lupus.
Systemic lupus erythematosus (SLE or lupus) is a severe autoimmune disorder that can adversely affect many organs, including the skin, kidney, blood and joints. This organ damage can result in substantial morbidity or even death. In patients suffering from lupus, their disease course is characterized by “flares” of increased disease activity that require treatment with aggressive immunosuppressive medications. Often, these flares can be heralded by the presence of a lupus rash. However, how this rash relates to systemic disease development remains unclear.
In most models of lupus, the onset of disease is a gradual process, and it has been difficult to model how a flare occurs. In her work, Dr. Kahlenberg has developed a model in which lupus-prone female mice develop a rapid flare of kidney disease following skin injury. In this project, Dr. Kahlenberg is studying the mechanisms by which skin injury can lead to a rapid flare of kidney inflammation. She will study the inflammatory cell populations present in the kidney and relate this to simultaneous changes in the skin and blood of the mice. Additionally, she will target the cytokine IL-18 to determine whether induction of flares of kidney inflammation by skin injury requires this cytokine. She anticipates this work will show that skin injury rapidly increases the inflammatory cell populations in the kidney and that blocking IL-18 may modulate this.
Potential: This work will benefit the scientific community by increasing knowledge of how the skin and kidney may cross-talk in lupus, thus leading to development of novel therapies that may help to prevent flares of lupus nephritis and reduce the need for immunosuppressive medications in lupus patients.
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