Abstract
Mice expressing the KRN T cell receptor transgene and the MHC class II molecule Ag7 (K/B×N mice) develop severe inflammatory arthritis, and serum from these mice causes similar arthritis in a wide range of mouse strains, owing to pathogenic autoantibodies to glucose-6-phosphate isomerase (GPI). This model has been useful for the investigation of the development of autoimmunity (K/B×N transgenic mice) and particularly of the mechanisms by which anti-GPI autoantibodies induce joint-specific imflammation (serum transfer model). In this chaper, after a summary of findings from this model system, we describe detailed methods for the maintenance of a K/B×N colony, crossing of the relevant TCR and MHC genes to other strain backgrounds, evaluation of KRN transgenic T cells, measurement of anti-GPI antibodies, induction of arthritis by serum transfer, and clinical and histological evaluation of arthritis.
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© 2007 Humana Press Inc., Totowa, NJ
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Monach, P. et al. (2007). The K/BxN Mouse Model of Inflammatory Arthritis. In: Cope, A.P. (eds) Arthritis Research. Methods in Molecular Medicine, vol 136. Humana Press. https://doi.org/10.1007/978-1-59745-402-5_20
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DOI: https://doi.org/10.1007/978-1-59745-402-5_20
Publisher Name: Humana Press
Print ISBN: 978-1-58829-918-5
Online ISBN: 978-1-59745-402-5
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