Increased Estrogen May Alter Immune Response
Systemic lupus erythematosus (SLE) is an autoimmune disease that is characterized by the production of autoantibodies that may cause tissue damage of target organs, such as the kidney. The B cells that secrete autoantibodies are generated in healthy individuals; however, they are unable to cause disease because the immune system is able to effectively regulate these cells. Dr. Christine Grimaldi is studying how the autoreactive B cells of SLE patients bypass the surveillance mechanisms of the immune system that would normally silence these cells in healthy individuals.
Since SLE affects females almost 10 times more frequently than males, it has been widely speculated that estrogen plays a role in disease progression. To learn more about the effects of estrogen on the regulation of B cells and the production of autoantibodies, Dr. Grimaldi has been treating mice with estrogen. The resultant data have shown that an increase in estrogen induces a lupus-like disease in treated mice.
These studies have important clinical implications since selective estrogen receptor modulators can be developed that specifically antagonize the estrogen receptor identified as being important for disease progression. Such clinically focused therapies may prove to be beneficial for treating patients with an estrogen responsive form of SLE