Author/Authors :
K. Rakhra، نويسنده , , Kavya and Bachireddy، نويسنده , , Pavan and Zabuawala، نويسنده , , Tahera and Zeiser، نويسنده , , Robert X. Xu، نويسنده , , Liwen and Kopelman، نويسنده , , Andrew T. Fan، نويسنده , , Alice C. and Yang، نويسنده , , Qiwei and Braunstein، نويسنده , , Lior and Crosby، نويسنده , , Erika and Ryeom، نويسنده , , Sandra and Felsher، نويسنده , , Dean W.، نويسنده ,
Abstract :
Summary
ne addiction is thought to occur cell autonomously. Immune effectors are implicated in the initiation and restraint of tumorigenesis, but their role in oncogene inactivation-mediated tumor regression is unclear. Here, we show that an intact immune system, specifically CD4+ T cells, is required for the induction of cellular senescence, shutdown of angiogenesis, and chemokine expression resulting in sustained tumor regression upon inactivation of the MYC or BCR-ABL oncogenes in mouse models of T cell acute lymphoblastic lymphoma and pro-B cell leukemia, respectively. Moreover, immune effectors knocked out for thrombospondins failed to induce sustained tumor regression. Hence, CD4+ T cells are required for the remodeling of the tumor microenvironment through the expression of chemokines, such as thrombospondins, in order to elicit oncogene addiction.
