Molecular abnormalities of the B cell in systemic lupus erythematosus are candidates for functional inhibition treatments

Abstract

Introduction: The B cell is a key player in the pathogenesis of systemic lupus erythematosus (SLE). Loss of B cell tolerance resulting in autoantibody production and immune complex formation and deposition are central features of the disease. B cell overactivity is a hallmark of SLE and molecular abnormalities in B cell signaling cascade have been described.

Areas covered: In this review, we will focus on the aberrant phenotype of B cell signaling in patients with lupus. We will also discuss data stemming from the use of small molecules that have recently been recognized to target important steps of the B cell signal transduction pathways with therapeutic implications for SLE.

Expert opinion: Attempts to target the B cell in SLE have been made through depletion, blocking of survival factors and co-receptor inhibition. However, the still unmet need for effective therapy of refractory disease makes the necessity for new drugs impelling.

Keywords::

• B cell
• Bruton's tyrosine kinase
• kinase inhibitor
• Lyn
• PI3K
• spleen tyrosine kinase
• systemic lupus erythematosus

Notes

This box summarizes key points contained in the article.