Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents

This Article Full Text Full Text (PDF, 580K) PPT slides of all figures Alert me when this article is cited Citation Map Services Email this article Similar articles in this journal Similar articles in PubMed Alert me to new content in the JEM Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Ettinger, R. Articles by McDevitt, H. O. Search for Related Content PubMed PubMed Citation Articles by Ettinger, R. Articles by McDevitt, H. O. Social Bookmarking                            What's this?

Brief Definitive Report

^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

© 2001 The Rockefeller University Press

CiteULike    Complore    Connotea    Del.icio.us    Digg    Facebook    Reddit    Technorati    Twitter    What's this?

This article has been cited by other articles:

• Grabner, R., Lotzer, K., Dopping, S., Hildner, M., Radke, D., Beer, M., Spanbroek, R., Lippert, B., Reardon, C. A., Getz, G. S., Fu, Y.-X., Hehlgans, T., Mebius, R. E., van der Wall, M., Kruspe, D., Englert, C., Lovas, A., Hu, D., Randolph, G. J., Weih, F., Habenicht, A. J.R. (2009). Lymphotoxin {beta} receptor signaling promotes tertiary lymphoid organogenesis in the aorta adventitia of aged ApoE-/- mice. JEM 206: 233-248 [Abstract] [Full Text]  
• Levisetti, M. G., Suri, A., Frederick, K., Unanue, E. R. (2004). Absence of Lymph Nodes in NOD Mice Treated With Lymphotoxin-{beta} Receptor Immunoglobulin Protects From Diabetes. Diabetes 53: 3115-3119 [Abstract] [Full Text]  
• Sung, H.-H., Juang, J.-H., Lin, Y.-C., Kuo, C.-H., Hung, J.-T., Chen, A., Chang, D.-M., Chang, S.-Y., Hsieh, S.-L., Sytwu, H.-K. (2004). Transgenic Expression of Decoy Receptor 3 Protects Islets from Spontaneous and Chemical-induced Autoimmune Destruction in Nonobese Diabetic Mice. JEM 199: 1143-1151 [Abstract] [Full Text]  
• Wu, Q., Fu, Y.-X., Sontheimer, R. D. (2004). Blockade of Lymphotoxin Signaling Inhibits the Clinical Expression of Murine Graft-versus-Host Skin Disease. J. Immunol. 172: 1630-1636 [Abstract] [Full Text]  
• Wu, Y., Han, B., Luo, H., Roduit, R., Salcedo, T. W., Moore, P. A., Zhang, J., Wu, J. (2003). DcR3/TR6 Effectively Prevents Islet Primary Nonfunction After Transplantation. Diabetes 52: 2279-2286 [Abstract] [Full Text]  
• Fava, R. A., Notidis, E., Hunt, J., Szanya, V., Ratcliffe, N., Ngam-ek, A., de Fougerolles, A. R., Sprague, A., Browning, J. L. (2003). A Role for the Lymphotoxin/LIGHT Axis in the Pathogenesis of Murine Collagen-Induced Arthritis. J. Immunol. 171: 115-126 [Abstract] [Full Text]  
• Kuai, J., Nickbarg, E., Wooters, J., Qiu, Y., Wang, J., Lin, L.-L. (2003). Endogenous Association of TRAF2, TRAF3, cIAP1, and Smac with Lymphotoxin beta Receptor Reveals a Novel Mechanism of Apoptosis. J. Biol. Chem. 278: 14363-14369 [Abstract] [Full Text]  
• Lu, T. T., Cyster, J. G. (2002). Integrin-Mediated Long-Term B Cell Retention in the Splenic Marginal Zone. Science 297: 409-412 [Abstract] [Full Text]  
• Luther, S. A., Bidgol, A., Hargreaves, D. C., Schmidt, A., Xu, Y., Paniyadi, J., Matloubian, M., Cyster, J. G. (2002). Differing Activities of Homeostatic Chemokines CCL19, CCL21, and CXCL12 in Lymphocyte and Dendritic Cell Recruitment and Lymphoid Neogenesis. J. Immunol. 169: 424-433 [Abstract] [Full Text]  

Home | Help | Feedback | Subscriptions | Archive | Search

TABLE OF CONTENTS