Joshy Jacob, PhD

Plasma cells are the terminally differentiated effector cells of the humoral arm of adaptive immunity. They can be short-lived with a half-life of two weeks or long-lived and persist for a lifetime. The mechanisms involved in the regulation of plasma cell function are not fully understood. Our studies have shown that CD28/B7 pathway is crucial for regulating plasma cell function. CD28, which is constitutively expressed on T cells, interacts with B7.1/B7.2 expressed on antigen-presenting cells is critical for T cell activation. CD28 is also expressed on murine and human plasma cells but its function on these cells remains unclear. We have demonstrated that CD28-deficieny in murine short- and long-lived plasma cells leads to increased survival and antibody production than their wildtype counterparts. Interestingly, plasma cells also express the ligand for CD28, B7.1/2. Surprisingly, deficiency of B7.1 and B7.2 in B cells also led to higher antibody levels, analogous to CD28^-/- plasma cells. Collectively, our results suggest that the CD28-B7 interaction operates as a key modulator of plasma cell function. Our current research is focused on understanding the mechanistic aspects of how CD28/B7 signals regulate plasma cell function.