Cellular immunity in systemic lupus erythematosus.
Production of pathogenic autoantibodies in patients with systemic lupus erythematosus (SLE) is the cornerstone in the pathogenesis of the disease. From the etiologic point of view, there is evidence that genetic, infectious, hormonal and environmental factors are essential to the development of SLE. The relative contribution of each group of factors to the expression of disease is individualized to each patient or group of patients with identical clinical disease. The cellular events which precede the B cell overactivity are crucial. T cells may produce excessive amounts of factors promoting B cell function, decreased amounts of suppressive factors or diminished cytotoxic ability to eliminate autoreactive T or B cells. The current understanding of lymphocyte and macrophage abnormalities are presented critically in this communication.
Boumpas
D T
DT
Kidney Disease Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892.
Eleftheriades
E G
EG
Tsokos
G C
GC
D001323:Autoantibodies / Q000096:biosynthesis; D001402:B-Lymphocytes / Q000276:immunology; D006801:Humans; D007111:Immunity, Cellular; D008180:Lupus Erythematosus, Systemic / Q000276:immunology*; D008264:Macrophages / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology
D001323:Autoantibodies