The latter two causes of death are becoming increasingly frequent as patients with SLE survive longer. The explanation for their increased frequency in SLE compared with normal individuals of comparable age and sex is not known. The etiology of SLE is unknown, but studies in humans and experimental models have provided a wealth of information regarding pathogenesis. The fundamental abnormality in SLE is B cell hyperactivity. Although abnormalities in T cell immunoregulation may contribute to disturbed B cell responsiveness, T cell dysfunction is not an invariant feature of the disease.
Genetic factors exert a modest influence on disease expression.
In view of the fact that 3 distinct murine models of SLE exist and that individual patients exhibit remarkable heterogeneity in symptoms, signs, and disease progression, it is reasonable to suppose that the pathogenetic factors influencing disease expression are heterogeneous, also. In this sense, SLE is a disease syndrome with diverse pathogenic factors resulting in variations in disease expression from patient to patient. Semin Arthritis Reum. Lupus as a renal disease. The reality and implications.