Aimee E Pugh-Bernard1, John C Cambier. 1. Integrated Department of Immunology, University of Colorado Health Sciences Center and National Jewish Medical Research Center, 1400 Jackson Street, Denver, CO 80206, USA.
Abstract
PURPOSE OF REVIEW: 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. RECENT FINDINGS: 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. SUMMARY: 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.
PURPOSE OF REVIEW: The purpose of this review is to inform the scientific community of the most recent findings surrounding B cell receptor signaling function in humansystemic lupus erythematosus and how altered B cell signaling may explain the characteristic hyperactivity of B cells in active disease and contribute to its pathogenesis. RECENT FINDINGS: 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. SUMMARY: The studies reviewed suggest that B cells from systemic lupus erythematosuspatients display molecular signaling defects that most likely contribute to pathogenesis of the disease and explain the characteristic hyperactivity of B cells in active disease.
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