The role of cytokines in systemic lupus erythematosus (SLE) glomerulonephritis is extremely complex. Proinflammatory molecules, such as TNF, IL-6, IL-1 and IL-18 are upregulated, as are both Thl and Th2 cytokines, with different implications: the local effects may be different from the systemic immunoregulatory ones. Excessive T helper cell function is a hallmark of SLE and abnormalities of Th citokine profiles have been implicated in loss of immune tolerance, increased antogenic load, defective B cell suppression and a variety of clinical manifestations. For some cytokines, TNF and IL-18 in particular, the local proinflammatory ones may be more relevant to the disease.