Monach Paul, Hattori Kimie, Huang Haochu, Hyatt Elzbieta, Morse Jody, Nguyen Linh, Ortiz-Lopez Adriana, Wu Hsin-Jung, Mathis Diane, Benoist Christophe
Section of Immunology and Immunogenetics, Joslin Diabetes Center, Boston, MA, USA.
Methods Mol Med. 2007;136:269-82. doi: 10.1007/978-1-59745-402-5_20.
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.
表达KRN T细胞受体转基因和II类主要组织相容性复合体分子A(g7)的小鼠（K/BxN小鼠）会发展出严重的炎性关节炎，并且这些小鼠的血清会在多种小鼠品系中引发类似的关节炎，这是由于针对葡萄糖-6-磷酸异构酶（GPI）的致病性自身抗体所致。该模型对于自身免疫性疾病发展（K/BxN转基因小鼠）的研究，特别是抗GPI自身抗体诱导关节特异性炎症的机制（血清转移模型）的研究很有用。在本章中，在总结该模型系统的研究结果后，我们描述了维持K/BxN群体、将相关TCR和MHC基因与其他品系背景杂交、评估KRN转基因T细胞、测量抗GPI抗体、通过血清转移诱导关节炎以及对关节炎进行临床和组织学评估的详细方法。
