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Systemic Versus Cartilage-Specific Expression of a Type II Collagen-Specific T-Cell Epitope Determines the Level of Tolerance and Susceptibility to Arthritis
Vivianne Malmström, Erik Michaëlsson, Harald Burkhardt, Ragnar Mattsson, Eero Vuorio and Rikard Holmdahl
Proceedings of the National Academy of Sciences of the United States of America
Vol. 93, No. 9 (Apr. 30, 1996), pp. 4480-4485
Published by: National Academy of Sciences
Stable URL: http://www.jstor.org/stable/39272
Page Count: 6
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Immunization of mice with rat type II collagen (CII), a cartilage-specific protein, leads to development of collagen-induced arthritis (CIA), a model for rheumatoid arthritis. To define the interaction between the immune system and cartilage, we produced two sets of transgenic mice. In the first we point mutated the mouse CII gene to express an earlier defined T-cell epitope, CII-(256-270), present in rat CII. In the second we mutated the mouse type I collagen gene to express the same T-cell epitope. The mice with mutated type I collagen showed no T-cell reactivity to rat CII and were resistant to CIA. Thus, the CII-(256-270) epitope is immunodominant and critical for development of CIA. In contrast, the mice with mutated CII had an intact B-cell response and had T cells which could produce γ interferon, but not proliferate, in response to CII. They developed CIA, albeit with a reduced incidence. Thus, we conclude that T cells recognize CII derived from endogenous cartilage and are partially tolerized but may still be capable of mediating CIA.
Proceedings of the National Academy of Sciences of the United States of America © 1996 National Academy of Sciences