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Regulators of B-cell activity in SLE: a better target for treatment than B-cell depletion?

Department of Rheumatology and Clinical Immunology, University Medical Center Groningen, Groningen, The Netherlands; Department of Nephrology, University Hospital Essen, University- Duisburg Essen, Germany

WH Abdulahad

Department of Rheumatology and Clinical Immunology, University Medical Center Groningen, Groningen, The Netherlands

M Bijl

Department of Rheumatology and Clinical Immunology, University Medical Center Groningen, Groningen, The Netherlands

CGM Kallenberg

Department of Rheumatology and Clinical Immunology, University Medical Center Groningen, Groningen, The Netherlandsc.g.m.kallenberg{at}int.umcg.nl

B cells, being a source of characteristic antinuclear autoantibodies, play a crucial role in the pathogenesis of systemic lupus erythematosus (SLE). Evidences indicate that alterations in B-cell regulation are responsible for B-cell hyperactivity as seen in SLE. T cells, soluble factors, and even B cells themselves regulate effector B-cell functions. The latter, so-called regulatory B cells possess regulatory function through production of the cytokine interleukin-10 (IL-10) that can damp down the humoral immune responses. This review will focus on B-cell regulation in the pathogenesis of SLE as a target for intervention. In particular, the regulatory impact of T cells through costimulation, soluble factors such as B lymphocyte stimulator, and the characteristics of IL 10–producing regulatory B cells will be discussed. Therapies targeting B cells as well as B-cell regulation seem promising, but the precise mechanisms involved in these interventions are not completely understood. More insight into B-cell regulation in SLE, and particularly in regulatory B cells, could lead to novel therapeutic strategies.

Key Words: B-cell regulation • SLE • IL-10

Lupus, Vol. 18, No. 7, 575-580 (2009)
DOI: 10.1177/0961203309102296


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