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The Journal of Immunology, 2003, 170: 4818-4825.
Copyright © 2003 by The American Association of Immunologists

Differential Contribution of IL-4 and STAT6 vs STAT4 to the Development of Lupus Nephritis1

Ram Raj Singh2,3,*, Vijay Saxena3,*, Song Zang3,{dagger}, Lily Li3,{dagger}, Fred D. Finkelman*, David P. Witte* and Chaim O. Jacob2,3,{dagger}

* University of Cincinnati College of Medicine, Departments of Internal Medicine and Pathology, Veterans Affairs Medical Center and Children’s Medical Center, Cincinnati, OH 45220; and {dagger} University of Southern California School of Medicine, Department of Medicine, Los Angeles, CA 90033

Mechanisms that initiate lupus nephritis and cause progression to end-stage renal disease remain poorly understood. In this study, we show that lupus-prone New Zealand Mixed 2410 mice that develop a severe glomerulosclerosis and rapidly progressive renal disease overexpress IL-4 in vivo. In these mice, STAT6 deficiency or anti-IL-4 Ab treatment decreases type 2 cytokine responses and ameliorates kidney disease, particularly glomerulosclerosis, despite the presence of high levels of IgG anti-dsDNA Abs. STAT4 deficiency, however, decreases type 1 and increases type 2 cytokine responses, and accelerates nephritis, in the absence of high levels of IgG anti-dsDNA Abs. Thus, STAT6 and IL-4 may selectively contribute to the development of glomerulosclerosis, whereas STAT4 may play a role in autoantibody production.


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