Figure 1.

Pathophysiologic mechanism of antibody production in SLE. Key events include defective apoptotic debris clearance, neutrophil extracellular trap (NET) formation, and dysregulated type I interferon signaling, which stimulate plasmacytoid dendritic cells and autoreactive B cells via TLRs. B cell tolerance breakdown, excess BAFF signaling, and abnormal T cell help (CD40L, IL-21, ICOS) drive germinal center responses, affinity maturation, and plasma cell formation. Long-lived plasma cells produce high-affinity autoantibodies, perpetuating immune complex formation and chronic inflammation. The cycle is sustained by genetic susceptibility, complement dysfunction, and impaired regulatory T cell control.