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In both collagen-induced arthritis (CIA) and rheumatoid arthritis, T cells recognize a galactosylated peptide from type II collagen (CII). In this study, we demonstrate that the CII259-273 peptide, galactosylated at lysine 264, in complex with Aq molecules prevented development of CIA in mice and ameliorated chronic relapsing disease. In contrast, nonglycosylated CII259-273/Aq complexes had no such effect. CIA dependent on other MHC class II molecules (Ar/Er) was also down-regulated, indicating a bystander vaccination effect. T cells could transfer the amelioration of CIA, showing that the protection is an active process. Thus, a complex between MHC class II molecules and a posttranslationally modified peptide offers a new possibility for treatment of chronically active autoimmune inflammation such as rheumatoid arthritis.

Type

Journal article

Journal

J Immunol

Publication Date

01/02/2006

Volume

176

Pages

1525 - 1533

Keywords

Animals, Arthritis, Experimental, Bystander Effect, Cattle, Chronic Disease, Collagen Type II, Galactose, Glycosylation, Histocompatibility Antigens Class II, Hybridomas, Immunodominant Epitopes, Immunotherapy, Active, Lymphocyte Activation, Male, Mice, Mice, Inbred BALB C, Multiprotein Complexes, Peptides, Rats, Solubility, T-Lymphocytes, Vaccines