Systemic lupus erythematosus (SLE) belongs to organ non-specific autoimmunedisorders. Similarly to other autoimmune diseases, SLE is also genetically determined. Among many genes involved in the predisposition to SLE those of the major histocompatibility complex (HLA) and the complement system (C2, C4, C1q, and MBP) have already been known for many years. Recently new genes were added to this list – the FcγRIIA gene (the receptor for Fc-fragment of IgG), the Fas and FasL genes involved in the regulation of apoptosis, and the TNF (tumour necrosis factor) gene. Hormones, especially oestrogens, substantially contribute to the pathogenesis of the disease as they stimulate lymphocytes to produce cytokines (IL-4, IL-6, IL-10) supporting antibody production by B-lymphocytes; moreover they suppress cellular immunity. SLE is a prototypic disease in which antibodies are responsible directly or indirectly, via immunocomplexes, for clinical symptoms. B cells are activated, thenumberofCD4+-lymphocytes is decreasedcompared todouble negativeT-lymphocytes (CD4-CD8-), the number of which is increased. Changes in the cytokine network are also observed, esp. increased levels of IFN-α, IL-4, IL-6, IL-2 receptor, and adhesive molecule ICAM-1 have been reported.

        Key words: autoantibodies, cytokines,HLA-complex,hormones,immunocomplexes, lymphocytes T and B