B cell receptor signaling in human systemic lupus erythematosus

Abstract

The purpose of this review is to inform the scientific community of the most recent findings surrounding B cell receptor signaling function in human systemic lupus erythematosus and how altered B cell signaling may explain the characteristic hyperactivity of B cells in active disease and contribute to its pathogenesis. B cell receptor signaling is abnormal in patients with active systemic lupus erythematosus as demonstrated by increased calcium flux and global B cell hyperactivity. Altered signaling has been explained by a variety of factors such as defective FcgammaRIIB signaling, decreased expression of the protein tyrosine kinase Lyn, and increased serum levels of B lymphocyte stimulator. The studies reviewed suggest that B cells from systemic lupus erythematosus patients display molecular signaling defects that most likely contribute to pathogenesis of the disease and explain the characteristic hyperactivity of B cells in active disease.