Cytokines and systemic lupus erythematosus

SLE is an autoimmune rheumatic disease that principally affects women in the childbearing years.1 The prevalence of SLE varies between ethnic groups, being approximately 1:250 among black women, 1:1000 in Chinese women and 1:4300 in white women. SLE affects the joints, skin and blood in over 80% of patients and the kidneys, central nervous system and cardiopulmonary system in 30%–50% of patients. Between 10% and 30% of patients have anticardiolipin antibodies that are associated with arterial and venous thrombosis. The majority of patients demonstrate systemic manifestations, which may include fatigue, malaise, fever, anorexia, nausea and weight loss. Many cytokines have been implicated in regulating disease activity and in the involvement of different organs in patients with SLE. This article reviews both the role of individual cytokines and discusses possible mechanisms of cytokine action in individual organs. Cytokine production in patients with SLE differs from both healthy controls and patients with other diseases such as rheumatoid arthritis (RA). It is important to note that cytokine production is not only changed in patients with SLE when compared with healthy controls but also changes with different disease phenotypes. For example, interleukin 6 (IL6) seems to be increased in the cerebrospinal fluid (CSF) of patients with central nervous system (CNS) involvement in SLE but not in patients with SLE who lack neurological symptoms.2 It may be that as in other inflammatory diseases, the balance of cytokines is more important in determining disease phenotype or severity rather than in determining disease susceptibility. Human CD4+ T-helper cells (Th) cells can be divided into four different subsets defined by their cytokine profile.3-5Th1 cells produce IL2, interferon γ (IFNγ) and tumour necrosis factor α (TNFα), Th2 cells produce IL4, IL5, IL6, IL10 (in mice) and IL13 and Th3 cells transforming growth factor β (TGFβ), …