The role of Tumor Necrosis Factor-alpha (TNF-α) in the pathogenesis of systemic lupus erythematosus

The Tumor Necrosis Factor-alpha (TNF-alpha) is a pleiotropic cytokine that produces different stimuli in various physiological and pathological conditions. TNF-alpha contributes importantly to the development of T cells, B cells, and dendritic cells. However, TNF-alpha is also a potent inflammatory mediator and apoptosis inducer. The significance of the TNF-alpha involvement in the pathogenesis of systemic lupus erythematosus (SLE) remains controversial. From the genetic standpoint, a number of studies suggest that the TNF-alpha gene polymorphism is involved in the susceptibility of SLE. Moreover, there is a close association between the TNF-alpha gene expression and clinical manifestations. In addition, the increased serum level of TNF-alpha is observed in SLE patients and associated with disease activity and certain systemic manifestations. Treatment with anti-TNF agents is, however, controversial in SLE since induction of antinuclear antibodies, anti-dsDNA, anticardiolipin antibodies, and cases of drug-induced lupus have been observed in rheumatoid arthritis patients. In this context, this study reviewed the importance of TNF-alpha in the pathogenesis of SLE. (C) 2011 Elsevier Ltd. All rights reserved.