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. 2007:136:269-82.
doi: 10.1007/978-1-59745-402-5_20.

The K/BxN mouse model of inflammatory arthritis: theory and practice

Paul Monach  1 , Kimie Hattori, Haochu Huang, Elzbieta Hyatt, Jody Morse, Linh Nguyen, Adriana Ortiz-Lopez, Hsin-Jung Wu, Diane Mathis, Christophe Benoist
Affiliations

The K/BxN mouse model of inflammatory arthritis: theory and practice

Paul Monach et al. Methods Mol Med. 2007.

Abstract

Mice expressing the KRN T cell receptor transgene and the MHC class II molecule A(g7) (K/BxN 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/BxN 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/BxN 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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