The Journal of Experimental Medicine
VeriKine-HS Human IFN-Beta
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Published online 4 June 2001.
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© The Rockefeller University Press, 0022-1007/2001/6/1333/ $5.00
The Journal of Experimental Medicine, Volume 193, Number 11, June 4, 2001 1333-1340

Brief Definitive Report

A Critical Role for Lymphotoxin-β Receptor in the Development of Diabetes in Nonobese Diabetic Mice

Rachel Ettingera, Sibyl H. Munsonb, Cheng-Chi Chaod, Mary Vadeboncoeurb, Jon Tomab, and Hugh O. McDevittb,c

a Basel Institute for Immunology, Basel CH-4005, Switzerland
b Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California 94305
c Department of Medicine, Stanford University School of Medicine, Stanford, California 94305
d Hyseq, Sunnyvale, California 94085
Dept. of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305-5124.650-723-9180650-725-4019

hughmcd{at}leland.stanford.edu

To assess the role of lymphotoxin-β receptor (LTβR) in diabetes pathogenesis, we expressed an LTβR–Fc fusion protein in nonobese diabetic (NOD) mice. The fusion protein was expressed in the embryo, reached high levels for the first 2 wk after birth, and then declined progressively with age. High expression of LTβR–Fc blocked diabetes development but not insulitis. After the decline in chimeric protein concentration, mice became diabetic with kinetics similar to the controls. Early expression of fusion protein resulted in disrupted splenic architecture. However, primary follicles and follicular dendritic cells, but not marginal zones, developed in aged mice. Hence, LTβR signaling is required for diabetes development and regulates follicular and marginal zone structures via qualitatively or quantitatively distinct mechanisms.

Key Words: autoimmune disease • tumor necrosis factor • LIGHT • lymphoid development • marginal zone

R. Ettinger and S. Munson contributed equally to this study.

© 2001 The Rockefeller University Press


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