Complete protection from relapsing experimental autoimmune encephalomyelitis induced by syngeneic B cells expressing the autoantigen
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Chen, CC
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UMDNJ, Robert Wood Johnson Med Sch, Dept Mol Genet Microbiol & Immunol, Piscataway, NJ 08854 USAUMDNJ, Robert Wood Johnson Med Sch, Dept Mol Genet Microbiol & Immunol, Piscataway, NJ 08854 USA
Chen, CC
[1
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Rivera, A
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UMDNJ, Robert Wood Johnson Med Sch, Dept Mol Genet Microbiol & Immunol, Piscataway, NJ 08854 USAUMDNJ, Robert Wood Johnson Med Sch, Dept Mol Genet Microbiol & Immunol, Piscataway, NJ 08854 USA
Rivera, A
[1
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Dougherty, JP
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UMDNJ, Robert Wood Johnson Med Sch, Dept Mol Genet Microbiol & Immunol, Piscataway, NJ 08854 USAUMDNJ, Robert Wood Johnson Med Sch, Dept Mol Genet Microbiol & Immunol, Piscataway, NJ 08854 USA
Dougherty, JP
[1
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Ron, Y
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UMDNJ, Robert Wood Johnson Med Sch, Dept Mol Genet Microbiol & Immunol, Piscataway, NJ 08854 USAUMDNJ, Robert Wood Johnson Med Sch, Dept Mol Genet Microbiol & Immunol, Piscataway, NJ 08854 USA
Ron, Y
[1
]
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[1] UMDNJ, Robert Wood Johnson Med Sch, Dept Mol Genet Microbiol & Immunol, Piscataway, NJ 08854 USA
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 (PLIP) 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. (C) 2004 by The American Society of Hematology.
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UNIV OXFORD,SIR WILLIAM DUNN SCH PATHOL,MRC,CELLULAR IMMUNOL UNIT,OXFORD OX1 3RE,ENGLANDUNIV OXFORD,SIR WILLIAM DUNN SCH PATHOL,MRC,CELLULAR IMMUNOL UNIT,OXFORD OX1 3RE,ENGLAND
DAY, MJ
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TSE, AGD
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UNIV OXFORD,SIR WILLIAM DUNN SCH PATHOL,MRC,CELLULAR IMMUNOL UNIT,OXFORD OX1 3RE,ENGLANDUNIV OXFORD,SIR WILLIAM DUNN SCH PATHOL,MRC,CELLULAR IMMUNOL UNIT,OXFORD OX1 3RE,ENGLAND
TSE, AGD
;
PUKLAVEC, M
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UNIV OXFORD,SIR WILLIAM DUNN SCH PATHOL,MRC,CELLULAR IMMUNOL UNIT,OXFORD OX1 3RE,ENGLANDUNIV OXFORD,SIR WILLIAM DUNN SCH PATHOL,MRC,CELLULAR IMMUNOL UNIT,OXFORD OX1 3RE,ENGLAND
PUKLAVEC, M
;
SIMMONDS, SJ
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UNIV OXFORD,SIR WILLIAM DUNN SCH PATHOL,MRC,CELLULAR IMMUNOL UNIT,OXFORD OX1 3RE,ENGLANDUNIV OXFORD,SIR WILLIAM DUNN SCH PATHOL,MRC,CELLULAR IMMUNOL UNIT,OXFORD OX1 3RE,ENGLAND
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UNIV OXFORD,SIR WILLIAM DUNN SCH PATHOL,MRC,CELLULAR IMMUNOL UNIT,OXFORD OX1 3RE,ENGLANDUNIV OXFORD,SIR WILLIAM DUNN SCH PATHOL,MRC,CELLULAR IMMUNOL UNIT,OXFORD OX1 3RE,ENGLAND
DAY, MJ
;
TSE, AGD
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UNIV OXFORD,SIR WILLIAM DUNN SCH PATHOL,MRC,CELLULAR IMMUNOL UNIT,OXFORD OX1 3RE,ENGLANDUNIV OXFORD,SIR WILLIAM DUNN SCH PATHOL,MRC,CELLULAR IMMUNOL UNIT,OXFORD OX1 3RE,ENGLAND
TSE, AGD
;
PUKLAVEC, M
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UNIV OXFORD,SIR WILLIAM DUNN SCH PATHOL,MRC,CELLULAR IMMUNOL UNIT,OXFORD OX1 3RE,ENGLANDUNIV OXFORD,SIR WILLIAM DUNN SCH PATHOL,MRC,CELLULAR IMMUNOL UNIT,OXFORD OX1 3RE,ENGLAND
PUKLAVEC, M
;
SIMMONDS, SJ
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UNIV OXFORD,SIR WILLIAM DUNN SCH PATHOL,MRC,CELLULAR IMMUNOL UNIT,OXFORD OX1 3RE,ENGLANDUNIV OXFORD,SIR WILLIAM DUNN SCH PATHOL,MRC,CELLULAR IMMUNOL UNIT,OXFORD OX1 3RE,ENGLAND