Regulatory T Cells in Graft-versus-Host Disease
移植物抗宿主病中的调节性 T 细胞
基本信息
- 批准号:7676416
- 负责人:
- 金额:$ 38.65万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2009
- 资助国家:美国
- 起止时间:2009-08-01 至 2014-07-31
- 项目状态:已结题
- 来源:
- 关键词:AcuteAddressAllogenicBloodCell DeathCell TransplantationCell TransplantsCellsCharacteristicsClinicalClonal AnergyClonal DeletionComplicationDataDevelopmentDiseaseGene ExpressionGenesGoalsHealthHematopoieticIL17 geneImmuneImmune responseImmunobiologyInstructionInterferon Type IIInterleukin-10LeadLifeMethodsMonitorMorbidity - disease ratePathway interactionsPatientsPeripheralPhenotypeProceduresProcessProphylactic treatmentQuality of lifeRecurrenceRegulationStagingSurvivorsT-LymphocyteTechnology AssessmentTestingTherapeutic InterventionTimeTransplant RecipientsTransplantationanergychronic graft versus host diseaseclinically significantexhaustiongraft vs host diseaseimprovedinsightmortalityregenerativetherapy duration
项目摘要
Graft-versus host disease (GVHD) is a major complication in recipients of allogeneic hematopoietic cell
transplants (HCT). This procedure can be life saving for otherwise fatal disease, however GVHD is
associated with significant morbidity and mortality. Fortunately, immunological tolerance occurs in a
majority of patients despite the.development of acute and chronic GVHD. Immune suppression therapy
(1ST) is administered to all patients at the time of transplantation, but the duration of therapy is variable.
Some patients can be withdrawn from 1ST within 6 months of HCT, but most require 1ST for 2-3 years.
Potential mechanisms for achieving peripheral tolerance include clonal deletion or exhaustion through
activation-induced cell death, development of clonal anergy or non-responsiveness, and development of
regulatory T cells (Treg) that suppress the immune response. Preliminary data shows that Treg expressing
the CD4+CD25+CD12710 phenotype are decreased in the blood of patients with active chronic GVHD
(cGVHD) on 1ST,and they tend to increase in patients with resolving cGVHD. Expression of the FoxpS
gene, a functional marker for regulatory T cells, is also decreased in patients with active cGVHD, but
expression levels tend to increase in tolerant patients. There are also other genes associated with immune
regulation such as IL10 that are found variably expressed in cGVHD patients. There are also genes
associated with T cell responder and effector functions such as IFNG and IL17 that are variably expressed
in patients with active GVHD and patients receiving 1ST.These preliminary data lead us to test the
hypothesis that multiple regulatory mechanisms are required for the control of GVHD. We will use micro
array technology for the assessment of global gene expression and address the following questions: (i)
identify the transcriptional profiles of T lymphocytes and selected subsets from HCT patients that are
associated with the different stages of cGVHD and with 1ST,and identify the genes and pathways that
distinguish patients with active cGVHD from patients achieving immunological tolerance; and (ii)
determine the functional characteristics and regenerative capacity of regulatory T cells in patients with
active and quiescent cGVHD and tolerant patients. Insight into the cellular changes occurring in patients
with active and resolving cGVHD may lead to better methods for monitoring GVHD activity and guiding the
use of 1ST,and suggest new strategies for facilitating the induction of tolerance.
RELEVANCE (See instructions):
The number of patients receiving allogeneic hematopoietic cell transplants and surviving otherwise fatal
disease continues to increase, however many of these patients continue to suffer from GVHD. The studies
proposed here are aimed at understanding the factors responsible for ongoing GVHD and the
mechanisms responsible for immunological tolerance. Understanding these processes may lead to more
effective therapeutic interventions, and improve the quality of life and health of transplant survivors.
移植物抗宿主病(GVHD)是异基因造血细胞受体的主要并发症
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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John Andrew Hansen其他文献
John Andrew Hansen的其他文献
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{{ truncateString('John Andrew Hansen', 18)}}的其他基金
Whole Genome Association Analysis of Hematopoietic Cell Transplant (HCT) Outcome
造血细胞移植 (HCT) 结果的全基因组关联分析
- 批准号:
8212026 - 财政年份:2011
- 资助金额:
$ 38.65万 - 项目类别:
Whole Genome Association Analysis of Hematopoietic Cell Transplant (HCT) Outcome
造血细胞移植 (HCT) 结果的全基因组关联分析
- 批准号:
8022984 - 财政年份:2011
- 资助金额:
$ 38.65万 - 项目类别:
Regulatory T Cells in Graft-versus-Host Disease
移植物抗宿主病中的调节性 T 细胞
- 批准号:
8309105 - 财政年份:2011
- 资助金额:
$ 38.65万 - 项目类别:
Whole Genome Association Analysis of Hematopoietic Cell Transplant (HCT) Outcome
造血细胞移植 (HCT) 结果的全基因组关联分析
- 批准号:
8424322 - 财政年份:2011
- 资助金额:
$ 38.65万 - 项目类别:
Whole Genome Association Analysis of Hematopoietic Cell Transplant (HCT) Outcome
造血细胞移植 (HCT) 结果的全基因组关联分析
- 批准号:
8603178 - 财政年份:2011
- 资助金额:
$ 38.65万 - 项目类别:
Whole Genome Association Analysis of Hematopoietic Cell Transplant (HCT) Outcome
造血细胞移植 (HCT) 结果的全基因组关联分析
- 批准号:
9389761 - 财政年份:2011
- 资助金额:
$ 38.65万 - 项目类别:
Biomarker Discovery in Chronic Graft-vs-Host Disease
慢性移植物抗宿主病的生物标志物发现
- 批准号:
8081764 - 财政年份:2008
- 资助金额:
$ 38.65万 - 项目类别:
Biomarker Discovery in Chronic Graft-vs-Host Disease
慢性移植物抗宿主病的生物标志物发现
- 批准号:
7881588 - 财政年份:2008
- 资助金额:
$ 38.65万 - 项目类别:
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