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增殖和非自主抑制胸腺细胞增殖，在控制胸腺大小方面发挥关键作用。TECs中RB-TS失活不影响T细胞的分化和成熟，表明TECs中RB-TS失活不足以破坏T细胞的发育。因此，为了增强各种患者的免疫功能，操纵tec作为一种治疗策略是非常尝试的。然而，长期灭活TECs中的RB-TS会对动物产生不利影响。我们已经完成了这个项目，目前正在准备发表稿件。宋旸，T.沙利文，k .克拉曼，d .吉尔伯特，T. N.奥沙利文，l .卢，D.C.海恩斯，J.凯勒和T.范戴克。基因工程小鼠胸腺细胞角蛋白18细胞RB失活导致淋巴样和间质增生障碍（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)