Non-redundant functions of type 3 innate lymphoid cells in mucosal immunity
3型先天淋巴细胞在粘膜免疫中的非冗余功能
基本信息
- 批准号:9902326
- 负责人:
- 金额:$ 48.3万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2019
- 资助国家:美国
- 起止时间:2019-04-01 至 2023-03-31
- 项目状态:已结题
- 来源:
- 关键词:AblationAddressAdultAnimalsArchitectureB-LymphocytesCell Differentiation processCell physiologyCellsCellular ImmunityCitrobacterCitrobacter rodentiumCytoprotectionDataDefectDevelopmentGeneticGenetic ModelsGut MucosaHelper-Inducer T-LymphocyteHomeostasisHost DefenseImmuneImmunityImmunologyInfectionInflammatoryInterleukin-17IntestinesKnockout MiceKnowledgeLamina PropriaLeadLymphocyteLymphoid CellMediatingMetabolismModelingMolecularMucosal ImmunityMucous MembraneMusPathologicPathway interactionsPeyer&aposs PatchesPhysiologyPlayProductionPublishingReportingRoleShapesSourceSurfaceT cell differentiationT cell responseT-Cell DepletionT-Cell DevelopmentT-LymphocyteTestingTimeadaptive immunitycell typecommensal bacteriacommensal microbescytokineenteric pathogengut microbiotahost microbiotaimmune functionimprovedinflammatory disease of the intestineinterleukin-22lymph nodesmicrobiotamortalitymouse modelmucosal microbiotanovelpreservationpreventresponsetranscription factor
项目摘要
Type 3 innate lymphoid cells (ILC3) perform multiple functions in host physiology. However, most of these
functions have been elucidated in the context of T cell depletion. There is an extensive overlap of regulatory
and functional networks between ILC3 and Th17 cells and how these two cell types contribute to immunity
is unclear. Identification of non-redundant functions of ILC3 has been impeded by the lack of ILC3 depletion
models that preserve normal T cell development and differentiation. To address this gap in knowledge, we
created the first model in which ILC3 development is prevented, but B and T cell development and T cell
differentiation is normal. Using this model we demonstrate a non-redundant function of ILC3 in mucosal
protection against an intestinal pathogen. We will examine the specific mechanism of this protection, as
well as identify novel T cell-independent functions of ILC3. Moreover, we will uncouple the role of LTi in
lymph node and Peyer’s patch development from the role of adult lamina propria ILC3. We will also
investigate the role of ILC3 in regulating homeostasis with the intestinal microbiota. Overall, our studies
will elucidate the cellular and molecular mechanisms controlling non-redundant ILC3 functions in both
maintaining a healthy gut and regulating infectious intestinal inflammation. We expect the results to lead
to the development of more specific strategies for targeting ILC3 and Th17 cells to improve intestinal
immune dysbalance or prevent pathologic intestinal inflammation.
3型先天淋巴样细胞(ILC3)在宿主生理学中执行多种功能。然而,其中大多数
在T细胞耗竭的背景下已经阐明了这些功能。有一个广泛的重叠监管
ILC3和Th17细胞之间的功能网络以及这两种细胞类型如何有助于免疫
还不清楚ILC3非冗余功能的鉴定受到缺乏ILC3耗竭的阻碍
保持正常T细胞发育和分化的模型。为了填补这一知识空白,我们
创建了第一个模型,其中ILC3的发展被阻止,但B和T细胞的发展和T细胞
分化正常。使用该模型,我们证明了ILC3在粘膜中的非冗余功能。
保护免受肠道病原体的侵害。我们将研究这种保护的具体机制,
以及鉴定ILC3的新的不依赖于T细胞的功能。此外,我们将解除LTi的作用,
淋巴结和派伊尔集合淋巴结的发育起成人固有层ILC3的作用。我们还将
研究ILC3在调节肠道微生物群的稳态中的作用。总的来说,我们的研究
将阐明控制非冗余ILC3功能的细胞和分子机制,
维持健康的肠道和调节感染性肠道炎症。我们希望结果能引领
开发针对ILC3和Th17细胞的更特异性策略,以改善肠道免疫功能,
免疫失衡或预防病理性肠道炎症。
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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Ivaylo Ivanov Ivanov其他文献
Ivaylo Ivanov Ivanov的其他文献
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{{ truncateString('Ivaylo Ivanov Ivanov', 18)}}的其他基金
Maintenance of mucosal homeostasis by commensal Th17 cells
共生 Th17 细胞维持粘膜稳态
- 批准号:
10621283 - 财政年份:2021
- 资助金额:
$ 48.3万 - 项目类别:
Maintenance of mucosal homeostasis by commensal Th17 cells
共生 Th17 细胞维持粘膜稳态
- 批准号:
10282976 - 财政年份:2021
- 资助金额:
$ 48.3万 - 项目类别:
Maintenance of mucosal homeostasis by commensal Th17 cells
共生 Th17 细胞维持粘膜稳态
- 批准号:
10462753 - 财政年份:2021
- 资助金额:
$ 48.3万 - 项目类别:
Discovery of immunomodulatory gut microbes with MAGIC
利用 MAGIC 发现免疫调节肠道微生物
- 批准号:
9808632 - 财政年份:2019
- 资助金额:
$ 48.3万 - 项目类别:
Non-redundant functions of type 3 innate lymphoid cells in mucosal immunity
3型先天淋巴细胞在粘膜免疫中的非冗余功能
- 批准号:
10374839 - 财政年份:2019
- 资助金额:
$ 48.3万 - 项目类别:
New mechanism of commensal bacteria interaction with host immunity
共生菌与宿主免疫相互作用的新机制
- 批准号:
9317868 - 财政年份:2017
- 资助金额:
$ 48.3万 - 项目类别:
Mechanisms of Mucosal Th17 Cell Induction By Segmented Filamentous Bacteria
分节丝状细菌诱导粘膜 Th17 细胞的机制
- 批准号:
8819130 - 财政年份:2013
- 资助金额:
$ 48.3万 - 项目类别:
Mechanisms of Mucosal Th17 Cell Induction By Segmented Filamentous Bacteria
分节丝状细菌诱导粘膜 Th17 细胞的机制
- 批准号:
10475627 - 财政年份:2013
- 资助金额:
$ 48.3万 - 项目类别:
Mechanisms of Mucosal Th17 Cell Induction By Segmented Filamentous Bacteria
分节丝状细菌诱导粘膜 Th17 细胞的机制
- 批准号:
8650824 - 财政年份:2013
- 资助金额:
$ 48.3万 - 项目类别:
Mechanisms of Mucosal Th17 Cell Induction By Segmented Filamentous Bacteria
分节丝状细菌诱导粘膜 Th17 细胞的机制
- 批准号:
9244017 - 财政年份:2013
- 资助金额:
$ 48.3万 - 项目类别:
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