The interplay between B and T cells in adaptive immunity is essential for production of anti-pathogen antibodies during infections and following vaccination. Similar pathways of T-B cell interactions likely lead to genesis of potentially pathogenic antibodies in autoimmunity. Mounting evidence suggests that in autoimmune diseases such as systemic lupus erythematosus (lupus), CD4+ T cells drive the generation of autoantibody-producing B cells via the germinal center (GC) reaction, with initiation of autoreactive B cell memory and long-lived plasma cell formation; however, the development and interaction of pathogenic T and B cells in comparison to the acute, pathogen-specific response are not well defined. My lab examines how adaptive immune cells provide protection against pathogens, but malfunction in the GC response in autoimmunity.