The Mechanism of Thymic Lymphomagenesis in Genetically Engineered Mouse Model
The Mechanism of Thymic Lymphomagenesis in Genetically Engineered Mouse Model
批准号:
8763391
负责人:
Terry van Dyke
金额:
$25.96万
依托单位国家:
美国
项目类别:
财政年份:
--
资助国家:
美国
项目状态:
未结题
起止时间:
至
关键词:
AddressAffectAnimalsApoptosisAstrocytesCDK4 geneCell CycleCell MaturationCell ProliferationCellsComplexCuesCyclinsCytokeratinCytokeratin 18DataDevelopmentDiseaseEndothelial CellsEpithelialFamily memberG1/S TransitionGenetic TranscriptionGenetically Engineered MouseGrowth FactorHematopoieticHematopoietic SystemHumanImmune systemLigandsLymphoidLymphomagenesisMalignant NeoplasmsManuscriptsMinorMusMyelogenousMyeloproliferationOrganPathway interactionsPatientsPhenotypePhosphorylationPlayPopulationPreparationProcessPublicationsRoleSignal TransductionStaining methodStainsT cell differentiationT-Cell DevelopmentT-LymphocyteTherapeuticThymic epithelial cellThymus GlandTumor Suppressionadaptive immunitybrain tissueimmune functionmouse modelreceptorthymocytetumorigenesis
中文摘要
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英文摘要
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)
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