Cytokines play a central role in the pathogenesis of systemic lupus erythematosus.

Excessive production of pathogenic autoantibodies is one of the hallmarks of systemic lupus erythematosus (SLE). The mechanisms that underlie this excessive production are still unclear. Although there is considerable evidence to suggest that both T cells and B cells play an important role in the etiology of SLE, convincing abnormalities at the T cell receptor or immunoglobulin gene loci have not been demonstrated. In this regard, because cytokines play such a pivotal role in the inflammatory response, a defect in the immunoregulation of B cells by cytokines should be considered as possible contender in disease etiology. The hypothesis that is proposed here is that multiple defects mediated by cytokines are present in individuals with lupus and that both cytokine production and the response of B cells to cytokines may be defective. These abnormalities could then be a central factor in the etiology of systemic lupus erythematosus.