Figure 1.

Proposed model for the pathogenesis of SLE describes the independent and yet interactive nature of the genes contributes to autoimmunity and end organ damage. I, Autoantibody production and activation of effector T cells and II, activation of susceptibility for end organ damage, can be initiated independently while they interact at different levels as indicated by pathways III and IV. Interaction of these pathways leads to end organ damage (Waters et al., 2004).