Unit

UNIT 15.22 The K/BxN Arthritis Model

  1. Paul A. Monach,
  2. Diane Mathis,
  3. Christophe Benoist

Published Online: 1 MAY 2008

DOI: 10.1002/0471142735.im1522s81

Current Protocols in Immunology

Current Protocols in Immunology

How to Cite

Monach, P. A., Mathis, D. and Benoist, C. 2008. The K/BxN Arthritis Model. Current Protocols in Immunology. 81:15.22:15.22.1–15.22.12.

Author Information

  1. Joslin Diabetes Center, Harvard Medical School, Boston, Massachusetts

Publication History

  1. Published Online: 1 MAY 2008
  2. Published Print: MAY 2008

Abstract

Mice expressing both the T cell receptor (TCR) transgene KRN and the MHC class II molecule Ag7 (K/BxN mice) develop severe inflammatory arthritis, and serum from these mice causes a similar arthritis in a wide range of mouse strains, due to autoantibodies recognizing glucose-6-phosphate isomerase (GPI). K/BxN transgenic mice have been useful for investigating the development of autoimmunity, and the serum transfer model has been particularly valuable in eliciting mechanisms by which anti-GPI autoantibodies induce joint-specific inflammation. This unit describes detailed methods for the maintenance of a K/BxN colony, induction of arthritis by serum transfer, clinical evaluation of arthritis, and measurement of anti-GPI antibodies. Curr. Protoc. Immunol. 81:15.22.1-15.22.12. © 2008 by John Wiley & Sons, Inc.

Keywords:

  • arthritis;
  • rheumatoid arthritis;
  • glucose-6-phosphate isomerase;
  • GPI;
  • anti-GPI;
  • serum transfer;
  • autoantibodies;
  • mouse model;
  • KRN;
  • K/BxN