B Cell Receptor Signaling in Human Systemic Lupus Erythematosus

Aimee E. Pugh-Bernard; John C. Cambier

Disclosures

Curr Opin Rheumatol. 2006;18(5):451-455. 

In This Article

Abstract and Introduction

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 FcγRIIB 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.

Introduction

Systemic lupus erythematosus (SLE) is a complicated autoimmune disease diagnosed on presentation of a variable subset of a wide array of clinical symptoms. The feature common to all SLE patients, however, is the presence of autoantibodies. Although self-reactive B cells produce the autoantibodies essential to the diagnosis of disease, B cells have proven in recent years to be active participants in the development of disease irrespective of autoantibody production. In light of this advancement, a central question surrounding the pathogenesis of the disease is whether intrinsic defects in SLE B cells play a role in triggering the immunological events that result in the onset of clinical disease. Although other immune cells play a role in SLE, B cells from SLE patients display signaling defects that may underlie pathogenesis and explain the characteristic hyperactivity of B cells in active disease. This article will present the current understanding of how B cell signaling plays a role in the pathogenesis and exacerbation of disease in human SLE.

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