关节炎
自身抗体
自身免疫
转基因
转基因小鼠
主要组织相容性复合体
免疫学
炎性关节炎
类风湿性关节炎
基因
化学
抗体
生物
抗原
生物化学
作者
Paul A. Monach,Kimie Hattori,Haochu Huang,Elzbieta Hyatt,Jody Morse,Linh T. Nguyen,Adriana Ortiz-Lopez,Hsin-Jung Wu,Diane Mathis,Christophe Benoist
出处
期刊:Methods in molecular medicine
日期:2007-01-01
卷期号:: 269-282
被引量:94
标识
DOI:10.1007/978-1-59745-402-5_20
摘要
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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