Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by widespread immunologic abnormalities and multiorgan involvement including the skin, joints, and kidney as well as the peripheral and central nervous systems. The clinical course of SLE is usually dependent on the organ involved such as neuropsychiatric syndromes of systemic lupus erythematosus (NPSLE), lupus nephritis (LN), lupus pancreatitis (LP), and pulmonary hypertension (PH). Early diagnosis and epoch-making therapeutic strategies are prerequisites for improved prognosis of patients with SLE. To fulfill this medical need, a better understanding of the pathogenesis of SLE is required. Research over the course of several years has yielded a basic scientific understanding of SLE pathogenesis. This includes understanding the role of various cytokines and chemokines in disease progression, the chronic activation of plasmacytoid dendritic cells by circulating immune complexes, and the expression of neutrophil-specific genes.