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Mediterr J Rheumatol 2015; 26(1): 68-69
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Molecular abnormalities of the B cell in Systemic Lupus Erythematosus are candidates for functional inhibition treatments
Stamatis-Nick Liosis, Konstantinos Melissaropoulos
Abstract
B lymphocytes are a key player of 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 this disease.  B cell overactivity is a hallmark of SLE and molecular abnormalities in B cell signaling cascade have been described.  Attempts to target the B cell in SLE have been made through depletion, blocking of survival factors and co-receptor molecule inhibition.  However, the still unmet need for effective therapy of refractory disease makes the necessity for new drugs impelling.  In this review, we will focus on the aberrant phenotype of B cell signaling in patients with lupus.  We will also refer to small molecules that have recently been recognized to target important steps of the B cell signal transduction pathways with therapeutic implications for SLE.  
Keywords: B cell, Bruton’s tyrosine kinase, kinase inhibitor, Lyn, PI3K, spleen tyrosine kinase, systemic lupus erythematosus