UC San Diego

The focus of this thesis is on the role of the B cell co- receptors CD19 and CD21 in the induction of B cell dependent autoimmunity. B cell dependent autoimmunity can be described as a process consisting of three fundamental steps; first is the generation of B cells that target self, second is the activation of these cells to produce pro- inflammatory soluble antibody (slg), and third is the deposition of this antibody on the target tissue where it initiates inflammation against self. Collectively, the first two steps in this process are functionally defined as the 'inductive phase' as they result in the production of auto-antibody that is sufficient to induce disease symptoms in a secondary recipients. The third step is referred to as the 'effector phase' of disease as it is the manifestation of the symptoms of inflammation that result from the downstream effector functions of auto- antibody production. This work addresses the roles that these two B cell co-receptors and their downstream phospholipid signaling play in both the generation and the activation of autospecific B cells; their roles in the inductive phase