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Journal of Biomedicine and BiotechnologyVolume 2011 2011, Article ID 432595, 14 pages

Review ArticleDivision of Pediatric Immunology, Department of Pediatrics, RWTH Aachen University, Pauwelsstraße 30, 52074 Aachen, Germany

Received 1 June 2011; Accepted 14 August 2011

Academic Editor: George Tsokos

Copyright © 2011 Kim Ohl and Klaus Tenbrock. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Systemic lupus erythematosus SLE is an autoimmune disease of unknown origin affecting virtually all organ systems. Beyond genetic and environmental factors, cytokine imbalances contribute to immune dysfunction, trigger inflammation, and induce organ damage. The key cytokine that is involved in SLE pathogenesis is interferon alpha. Interferon secretion is induced by immune complexes and leads to upregulation of several inflammatory proteins, which account for the so-called IFN signature that can be found in the majority of SLE PBMCs. Additionally IL-6 and IFN-y as well as T-cell-derived cytokines like IL-17, IL-21, and IL-2 are dysregulated in SLE. The latter induce a T-cell phenotype that is characterized by enhanced B-cell help and enhanced secretion of proinflammatory cytokines but reduced induction of suppressive T cells and activation-induced cell death. This paper will focus on these cytokines and highlights pathophysiological approaches and therapeutic potential.

Autor: Kim Ohl and Klaus Tenbrock



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