Publications

Abstract

Effective B cell mediated immunity, including the formation of germinal centers and the generation of high affinity memory B cells and long-lived plasma cells, is dependent on help provided by CD4+ T cells. Immunodeficiencies that present with defects in the antibody response have provided us with insight into the molecular mechanisms involved in generation of B cell responses and the provision of T cell help. Once such disorder is XLP, which was found to result from mutations in SH2D1A the gene encoding SAP. Patients with XLP present with humoral defects characterized by hypogammaglobulinemia. We now know that SAP, signaling downstream of multiple members of the SLAM family of cell surface receptors, plays a crucial role in many aspects of this immune response. Here, we discuss the role of SAP in the generation of humoral immunity, particularly T-dependent antibody responses and the generation of germinal centers.