Phenotypic characterization of itm2a-deficiency in T cells
Phenotypic characterization of itm2a-deficiency in T cells
批准号:
8227163
负责人:
I-CHENG HO
金额:
$8.69万
依托单位国家:
美国
项目类别:
财政年份:
2012
资助国家:
美国
项目状态:
已结题
起止时间:
2012-02-15 至 2014-01-31
关键词:
AffectAntibodiesAutoimmune DiseasesBacteriaBiological MarkersBiologyCell Differentiation processCellsClinicalDataDevelopmentDiseaseGene TargetingGoalsImmuneIntegral Membrane ProteinInvadedLaboratoriesLeadLeukocytesLupusMediatingMolecularMouse StrainsMultiple SclerosisMusOrganPathway interactionsPeripheralPhenotypePhysiologicalPlayProcessProteinsPsoriasisPublishingReagentRheumatoid ArthritisRoleSurfaceT-LymphocyteTh2 CellsTherapeuticThymocyte DevelopmentViruscrosslinkneoplastic cellnovelpathogentherapeutic targetthymocytetranscription factor
中文摘要
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英文摘要
DESCRIPTION (provided by applicant): T lymphocytes (T cells) are a subset of white blood cells and are essential for eradicating invading bacteria, virus, and tumor cells. However, T cells can also initiate and propagate many autoimmune diseases, such as rheumatoid arthritis, multiple sclerosis, psoriasis, and lupus, if their function is not regulated properly. Better understanding of how the development and function of T cells is regulated can lead to novel treatments for many diseases. Preliminary data gathered at Dr. Ho's laboratory has suggested that a novel protein, namely itm2a, plays a critical role in regulating the development and function of T cells. In this project, Dr. Ho's team plans to study the impact of itm2a deficiency on T cells. Results generated from this project will establish itm2a as a rich therapeutic target in many clinical settings.
PUBLIC HEALTH RELEVANCE: Targeting T cells is therapeutic in many clinical settings. The molecular mechanism regulating the development and function of T cells is a very complicate process and still not fully understood. Published and our preliminary data have strongly suggested that the integral membrane protein itm2a plays a critical role in regulating the development and function of T cells. However, the physiological function of itm2a is largely unknown. The immediate goal of this project is to characterize the phenotype of T cells and mice that are made deficient in itm2a. Data generated from this project may uncover a novel pathway regulating the development and function of T cells.
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