This review summarises a number of current insights into the pathogenesis of SLE. On the basis of the interaction of environmental factors within a predisposed host, a chronic autoimmune process gains function with a positive feed-forward loop between innate and adaptive immunity. A current focus of SLE pathogenesis is on the enhanced production of certain cytokines, such as type I interferons and BLyS/BAFF, suggesting continuous plasmacytoid dendritic and myeloid cell activity together with disturbances of B lineage cells (increased autoantibodies, including anti-dsDNA and plasmablasts, which correlate with SLE activity and memory B-cell abnormalities). Recent studies provided evidence that CD4+ and CD8+ T cells and B cells are hyporesponsive in SLE, likely reflecting their 'post-activation status'. Data of enhanced protein tyrosine phosphatase activity of lymphocytes in SLE require consideration if they represent a disease characteristic. Better understanding of the chronic autoimmune phase is needed in addition to those phases during flares and will permit improved treatment of SLE.
Keywords: B cells; Etiopathogenesis; IL-2 deficiency; Inflammation; Interferon; SLE; TLR.
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