Research in the Satterthwaite lab focuses on understanding the signals that control B lymphocyte development and function. B cells are critical for normal immune responses. Each B cell is equipped with a receptor that allows it to bind to a unique antigen. When B cells encounter the antigen for which they are specific, they become activated and differentiate into plasma cells. These plasma cells secrete antibodies that can bind to the antigen and target it for destruction.
During an infection, those B cells whose antigen receptors recognize the invading pathogen will produce pathogen-specific antibodies that help clear the infection. Because antibodies can cause damage, B cells that recognize one’s self are normally either eliminated or inactivated in a process called B cell tolerance. However, in autoimmune diseases such as lupus, these tolerance mechanisms are impaired and autoantibodies are produced. These can cause inflammation and tissue damage and lead to organ failure.
Thus, understanding the molecular mechanisms that control B cell tolerance, activation and differentiation into antibody secreting plasma cells has important implications for both vaccine design and the development of therapies for autoimmune disease.