The Journal of Experimental Medicine
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Published online 4 June 2001.
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© The Rockefeller University Press, 0022-1007/2001/6/1327/ $5.00
The Journal of Experimental Medicine, Volume 193, Number 11, June 4, 2001 1327-1332

Brief Definitive Report

Reversal of Spontaneous Autoimmune Insulitis in Nonobese Diabetic Mice by Soluble Lymphotoxin Receptor

Qiang Wua, Benoît Salomona,b, Min Chena, Yang Wanga, Lisa M. Hoffmana, Jeffrey A. Bluestonea,b, and Yang-Xin Fua

a Committee on Immunology and the Department of Pathology, University of Chicago, Chicago, Illinois 60637
b Ben May Institute for Cancer Research, University of Chicago, Chicago, Illinois 60637
Department of Pathology and Immunology, University of Chicago, 5841 S. Maryland, Rm. J541, MC3083, Chicago, IL 60637.773-834-8940773-702-0929

yfu{at}midway.uchicago.edu

One striking feature of spontaneous autoimmune diabetes is the prototypic formation of lymphoid follicular structures within the pancreas. Lymphotoxin (LT) has been shown to play an important role in the formation of lymphoid follicles in the spleen. To explore the potential role of LT-mediated microenvironment in the pathogenesis of insulin-dependent diabetes mellitus (IDDM), an LTβ receptor–immunoglobulin fusion protein (LTβR–Ig) was administered to nonobese diabetic mice. Early treatment with LTβR–Ig prevented insulitis and IDDM, suggesting that LT plays a critical role in the insulitis development. LTβR–Ig treatment at a late stage of the disease also dramatically reversed insulitis and prevented diabetes. Moreover, LTβR–Ig treatment prevented the development of IDDM by diabetogenic T cells in an adoptive transfer model. Thus, LTβR–Ig can disassemble the well established lymphoid microenvironment in the islets, which is required for the development and progression of IDDM.

Key Words: adhesion molecule • autoimmune diabetes • insulitis • lymphotoxin • lymphotoxin β receptor

Q. Wu and B. Salomon contributed equally to this study. Drs. Bluestone and Fu should both be considered senior authors of this article.

© 2001 The Rockefeller University Press


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