Abstract
THE term immune-complex disease describes a state in which circulating antigen–antibody complexes, formed by coexisting immune reactants, induce vascular injury. In this presentation I will review evidence that immune complexes are responsible for the development of glomerulonephritis in systemic lupus erythematosus (SLE), and analyze the variables affecting the pathogenesis of an experimental model (chronic serum sickness) that, in many respects, resembles SLE nephritis. Systemic Lupus Erythematosus Clinical Features At the outset, it is appropriate to comment on the clinical and pathological features of the syndrome as we now recognize them and to compare them with the picture of SLE 20 . . .
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