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Abstract
systemic lupus erythematosus (SLE) is a relatively common autoimmune disease characterized by autoantibody production against a variety of nuclear antigens and multiple end organ damage. Antinuclear antibodies are thought to act directly in the pathogenesis of the disease, but the mechanisms underlying their production are ill defined.
Production of autoantibody to cellular macromolecule is a central immunological disturbance in SLE .Polycolonal B cell activation and auto antigen driven immunological stimulation, are thought to be responsible for the production of auto- antibodies in SLE. Furthermore many genetic and environmental factors may contribute to its pathogenesis.
Cytokines are usually extra-cellular signaling proteins, they are produced by many different cell types that are involved in cell-to-cell interactions. In many inflammatory diseases such as SLE and rheumatoid arthritis, it seems that the balance between pro-inflammatory and anti-inflammatory cytokines determines the degree and extent of inflammation and thus can lead to major clinical effects.
Future therapy might be targeted to specific suppression of the production of autoantibodies as a measure to suppress the clinical activity of SLE. So treatments that alter cytokines release and thus reduce inflammatory and immune responses, should be more effective and should have fewer adverse effects than the broadly immunosuppressive therapies used now.