Successful vaccines (e.g., polio, yellow fever) rely upon antibodies to confer long-lasting immunity against the pathogen. Influenza virus, which rapidly accrues mutations in its surface glycoproteins, remains elusive to the traditional vaccination strategies. These mutations, termed “antigenic drift”, are the impetus for seasonal revision of the vaccine. It is believed that the first virus encountered early in life conditions lifelong immunity – a phenomenon called “original antigenic sin” or “imprinting”. Understanding how immune history (i.e., existence of Bmem) affects the production of new antibodies to the same or similar antigen is crucial for the development of new vaccines.
B cell receptor recognition
When B cells are “good” they can distinguish friend from foe: producing antibodies that initially eliminate infection and can subsequently “remember” such a foe, thus providing long-lasting protection through immune memory. However, when B cells are “bad”, they can cause autoimmune diseases and cancer. Since B cell behavior is initiated, and ultimately controlled through the B cell antigen receptor (BCR), understanding the fundamental differences between the good and the bad B cells requires a detailed molecular understanding of the BCR and its signaling components.