الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
Systemic lupus erythematosus is an immune mediated disease which can affect many different organ systems. It is a primary auto immune disease in which the body loses self-tolerance towards autoantigens and mounts an inappropriate attack on various target tissue of the body.
The etiology of the disease is multi factorial involving genetic, immunological disorder, viral infection, hormonal and ultraviolet light modulation.
The pathology can be attributed to autoantibody binding, immune complex deposition or cell mediated immunity.
Cytokines, as small soluble proteins secreted by cells after activation, can play key roles in the regulation of systemic inflammation, local tissue damage and immunomodulation.
These cytokines may exert either pro-inflammatory or anti-inflammatory effects or both, depending on specific local microenvironments. The abnormalities of various cytokines may reflect the imbalance among different immune cell subsets, such as Th1/Th2 and Treg, thus contributing greatly to SLE pathogenesis.
Interleukin 10 has an important role in the growth, survival, differentiation and function of B cells. Abnormally increased IL 10 synthesis seems contributing to the spontaneous hyperactivity of the B cell compartment, so that it can directly result in autoantibody production by committed plasma cells, circulating immune complex formation and tissue damage associated with SLE.