The roles of interleukin-6 and interleukin-10 in B cell hyperactivity in systemic lupus erythematosus

Systemic lupus erythematosus (SLE) is an autoimmune disease most prevalent in women between the ages of twenty and sixty. Successful treatment remains challenging due to a lack of understanding of the underlying mechanisms and multiple symptoms ranging from skin rashes to glomerulonephritis. The pathogenesis of SLE has been linked to a B-cell hyperproliferation unique to afflicted patients. These B-cells generate large quantities of IgG autoantibodies, ultimately capable of leading to lupus nephritis and renal failure. The significance of cytokines in SLE and in murine lupus, a related disease in mice, has been debated, particularly with respect to B-cell activity. Potential roles of auto-regulatory and inflammatory cytokines have been investigated. In particular, IL-6 and IL-10 have been shown to be key factors in regulating autoantibody-secreting B-cell activity in lupus. Here, we will provide a critical overview of our current knowledge of the regulatory roles of these two cytokines in SLE.