Evaluation of signals mediating beta-cell regeneration
介导 β 细胞再生的信号评估
基本信息
- 批准号:8883807
- 负责人:
- 金额:$ 33.63万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2015
- 资助国家:美国
- 起止时间:2015-04-01 至 2020-03-31
- 项目状态:已结题
- 来源:
- 关键词:AddressAdoptive TransferAdultApoptoticAreaAutoimmune DiseasesAutoimmune ProcessAutoimmunityBeta CellBiologyBlood GlucoseCD3 AntigensCell ProliferationCell TherapyCellsCoculture TechniquesDiabetes MellitusElementsEnsureEnvironmentEvaluationExperimental ModelsFailureFutureGenerationsGenetic Predisposition to DiseaseGoalsHumanImmunogeneticsImmunosuppressive AgentsImmunotherapyIn VitroInbred NOD MiceInflammationInjuryInsulinInsulin-Dependent Diabetes MellitusMediatingModelingMolecular ProfilingMusNatural regenerationPancreasPatientsPhenotypePhysiologicalPredispositionPublishingRecoveryReportingResearchResearch PersonnelRoleSignal TransductionSyndromeTestingTherapeuticWorkdesigndiabeticdifferential expressionfeedingin vivoin vivo regenerationisletmacrophagemeetingsmonocyteperipheral bloodpreventpublic health relevanceregenerativerelease factorrepairedresearch study
项目摘要
DESCRIPTION (provided by applicant): Type 1 diabetes is a syndrome defined by high blood glucose levels caused by reduction in number of insulin producing cells, thus a cure for diabetes should entail replacement of ß-cells. There is a genetic predisposition for autoimmune susceptibility regarding macrophage phenotype in NOD mice and human T1D-patients, which contributes to persistence of inflammation, and ß-cell destruction. Here, we provide evidence that macrophages are important elements of pancreatic regeneration in general, and ß-cell generation in particular. Furthermore, we demonstrate that macrophages isolated from the NOD strain have an inherent inability to induce ß-cell generation. In this proposal, we will test the central hypothesis that Type1 diabetes is the combined effect of autoimmunity and the inability of macrophages to generate a cellular phenotype important for ß-cell regeneration. The experimental models described in this proposal will allow us to further study the macrophage-dependent ß-cell proliferation in mice (specific aims 1), to evaluate the ability of human-derived
macrophages to induce ß- cell replication (specific aims 2), and to identify putative factors released by macrophages that are necessary for human ß-cell generation (specific aims 3). Immune therapy significantly reduces the autoimmune-associated ß-cell proliferation. Thus, additional therapeutic approaches that would stimulate ß-cell regeneration in the absence of autoimmune destruction may be needed for recovery of ß-cell mass. As a potential cell therapeutic approach, macrophages generated from patient's monocytes could be reprogrammed to promote ß-cell regeneration. This work is a high priority area as it is directly applicable to our full understanding and potential treatment of T1D.
项目成果
期刊论文数量(0)
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FARZAD ESNI其他文献
FARZAD ESNI的其他文献
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{{ truncateString('FARZAD ESNI', 18)}}的其他基金
Evaluation of the Effect of Autoimmunity on Acinar-Derived Insulin Producing Cells
自身免疫对腺泡源性胰岛素产生细胞影响的评价
- 批准号:
10185387 - 财政年份:2021
- 资助金额:
$ 33.63万 - 项目类别:
Evaluation of the Effect of Autoimmunity on Acinar-Derived Insulin Producing Cells
自身免疫对腺泡源性胰岛素产生细胞影响的评价
- 批准号:
10374892 - 财政年份:2021
- 资助金额:
$ 33.63万 - 项目类别:
Chemical pancreatectomy for chronic pancreatitis and pancreatic cancer
化学胰腺切除术治疗慢性胰腺炎和胰腺癌
- 批准号:
10163180 - 财政年份:2019
- 资助金额:
$ 33.63万 - 项目类别:
Chemical pancreatectomy for chronic pancreatitis and pancreatic cancer
化学胰腺切除术治疗慢性胰腺炎和胰腺癌
- 批准号:
10403513 - 财政年份:2019
- 资助金额:
$ 33.63万 - 项目类别:
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