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Rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) are multifactorial autoimmune diseases that originate from the patient’s excessive immune and inflammatory response to a pathogenic agent (that is, an infective antigen).1
The pathophysiological mechanisms are activated after the combination of several predisposing factors, which include the relations between histocompatibility epitopes and epitopes of the pathogenic antigen, the altered status of the stress response system (hypothalamic-pituitary-adrenocortical axis = HPA) and the gonadal hormone pattern (hypothalamic-pituitary-gonadal axis = HPG), with oestrogens principally implicated as enhancers of the immune response, and androgens and progesterone as natural suppressors (fig1).2-8
An intricate balance with bidirectional interactions between soluble mediators, released by the neuroendocrine system (that is, steroid hormones and neuropeptides) and products of activated cells of the immune/inflammatory system (cytokines) maintains the homeostasis in presence of the immune/inflammatory stimulus.9-12
Cytokine patterns and sub-patterns in RA and SLE
Cytokine secretion seems fundamental in determining the duration and intensity of an immune response, and how steroid hormones (gonadal and adrenal steroids) influence autoimmunity may entail a further balance between Th1 and Th2 lymphocyte responses.13-15
Th1 lymphocytes produce mainly interleukin 2 (IL2) and interferon γ (IFNγ) and are primarly responsible for cell mediated immunity, while Th2 lymphocytes produce mainly IL4, IL5, IL13, and IL10, and are responsible for humoral immunity, supporting the activation of immunoglobulin secreting cells (fig 2).16 17