Leading the way to a cure


Function of TNFAIP3/A20 Genetic Variants in SLE

Ma, Averil, MD, PhD

University of California, San Francisco

Although we still don’t know what causes lupus, recent genetic studies have provided important clues. For instance, Averil Ma, MD, PhD, of the University of California-San Francisco, and his team have found that mutations in and around the A20 gene are associated with the risk of developing SLE. They also discovered that A20 is a powerful anti-inflammatory protein that prevents spontaneous inflammation. 

The team has recently created a new mouse model in which A20 is removed from B lymphocytes, the immune cells that help make the autoantibodies that cause disease in lupus. They found that these mice spontaneously develop several characteristics of human lupus.

Based on these findings, Dr. Ma and his team plan to use their grant to better understand how A20 predisposes people to develop lupus. First, they will examine A20 expression levels and A20 dependent functions in lymphocytes from people with lupus. They will then test blood cells from these individuals and correlate these findings with genetic analyses. The team will also study the development of lupus in their genetically modified mice.

What this study means for people with lupus: This proposal represents a unique opportunity to dramatically enhance our understanding of how A20 causes SLE. This understanding will help researchers identify specific compounds that could prevent SLE, possibly moving the field closer to developing effective treatments. 

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