The Mechanism of Thymic Lymphomagenesis in Genetically Engineered Mouse Model

我们的数据表明，Rb通过自主抑制TECs的增殖和非自主抑制胸腺细胞的增殖，在控制胸腺大小方面发挥了关键作用。TECs中RB-TS失活不影响T细胞的分化和成熟，提示TECs中RB-TS失活不足以干扰T细胞的发育。因此，将TECs作为一种治疗策略来提高各种患者的免疫功能是非常有尝试的。然而，在TECs中长期失活RB-TS将对动物产生不利影响。我们已经完成了这个项目，目前正在准备出版手稿。首页--期刊主要分类--期刊细介绍--期刊题录与文摘--期刊详细文摘内容胸腺细胞角蛋白18细胞中Rb失活导致基因工程小鼠淋巴样和间质增殖性疾病(准备中)

Our data show that RB plays a critical role on controlling thymus size by suppressing TECs proliferation cell-autonomously, and also thymocytes proliferation cell non-autonomously. T cell differentiation and maturation were not affected by RB-TS inactivation in TECs, suggesting that RB-TS inactivation in TECs is not sufficient to disrupt T cell development. Thus, it is very attempting to manipulate TECs as a therapeutic strategy in order to enhance the immune function in a wide variety of patients. However, long term inactivating RB-TS in TECs will have detrimental effect on animals. We have finished this project and are currently in the process of preparing the manuscript for publication. Y. Song, T.Sullivan, K.Klarmann, D.Gilbert, T. N. O'Sullivan, L.Lu, D.C. Haines, J. Keller, and T. Van Dyke. Inactivation of RB in thymic cytokeratin 18 cells results in lymphoid and stromal proliferative disorder in genetically engineered mice (in preparation)