SEARCH:   Advanced

Blood, 15 June 2004, Vol. 103, No. 12, pp. 4616-4618. Prepublished online as a Blood First Edition Paper on February 26, 2004; DOI 10.1182/blood-2004-01-0091. This Article Full Text Full Text (PDF) All Versions of this Article: 2004-01-0091v1 103/12/4616    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Chen, C.-C. Articles by Ron, Y. Search for Related Content PubMed PubMed Citation Articles by Chen, C.-C. Articles by Ron, Y. Related Collections Immunotherapy Brief Reports Immunobiology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Brief report Complete protection from relapsing experimental autoimmune encephalomyelitis induced by syngeneic B cells expressing the autoantigen Chiann-Chyi Chen, Amariliz Rivera, Joseph P. Dougherty, and Yacov Ron From the Department of Molecular Genetics, Microbiology, and Immunology, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Piscataway, NJ. Experimental autoimmune encephalomyelitis (EAE), an animal model for human multiple sclerosis (MS), is a typical CD4+ T-cell-mediated autoimmune disease of the central nervous system (CNS) characterized by perivascular inflammation culminating in focal demyelinations. Like MS, EAE induced by proteolipid protein (PLP) usually follows the form of a relapsing-remitting disease. We have previously described an immunotherapy model in which infusion of autologous B cells expressing the PLP encephalitogenic determinant induced PLP-specific unresponsiveness and protected mice from induction of EAE. Here we show that the same treatment when initiated after disease onset, which resembles the clinical situation presented in MS, completely protects all treated animals from further relapses. We also show that protected animals were unresponsive to PLP as measured by delayed-type hypersensitivity (DTH). This represents a novel immunotherapeutic approach that can be exploited to develop treatments for human MS and other T-cell-mediated autoimmune diseases. (Blood. 2004;103:4616-4618) CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: M. Werner-Klein, C. Dresch, P. Marconi, and T. Brocker Transcriptional Targeting of B Cells for Induction of Peripheral CD8 T Cell Tolerance J. Immunol., June 15, 2007; 178(12): 7738 - 7746. [Abstract] [Full Text] [PDF]

	Blood Online is supported in part by Genentech BioOncology and Biogen Idec
	Copyright © 2004 by American Society of Hematology         Online ISSN: 1528-0020