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
基本信息
- 批准号:9317868
- 负责人:
- 金额:$ 24万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2017
- 资助国家:美国
- 起止时间:2017-02-01 至 2019-01-31
- 项目状态:已结题
- 来源:
- 关键词:AdherenceAdhesionsAntigen-Presenting CellsAntigensBacteriaBacterial AntigensBacterial ProteinsBiological ProcessCD4 Positive T LymphocytesCarrier ProteinsCell membraneCellsClathrinCollectionCommunicationCytoplasmEndocytic VesicleEndocytosisEpithelialEpithelial CellsEukaryotic CellFecesGastrointestinal tract structureGenerationsGram-Negative BacteriaHumanImmune responseImmunityIn VitroIndividualInflammationInjection of therapeutic agentIntestinesMediatingMediator of activation proteinMembraneMicrobeMolecularMorphologyMouse StrainsMucosal ImmunityMucous MembraneMucous body substanceNatureOrganismPathway interactionsPeptidesPhagocytosisPhysiologicalPlayProcessProductionProteinsReactive Oxygen SpeciesRoleRouteSecretory Immunoglobulin ASurfaceSymbiosisSynapsesSystemT-LymphocyteTissuesToxinVesicleVirusantimicrobialchemical geneticscommensal microbescytokineexperimental studygenetic approachglycosylationimmunoregulationin vivoinnate immune functioninterestintestinal homeostasismicrobialmicrobiotanovelpathogenprotein transportreceptorresponsetool
项目摘要
How commensal bacteria communicate with the host to modify immunity is incompletely understood.
Here we propose to characterize a previously unrecognized pathway of communication between bacteria
and the eukaryotic host and its role in mediating immunomodulatory effects of mucosa-associated
commensals. To identify the nature of the process we will characterize the involvement and requirement
of various endocytic pathways by a combination of chemical and genetic approaches. We will also
generate and examine these interactions in a novel in vitro system.
If successful, our studies will uncover a novel mechanism for delivery of bacterial antigens for
activation of commensal-specific T cells in the intestine, and/or for delivery of bacterial molecules for
immune modulation.
共生细菌如何与宿主沟通以改变免疫力,目前还不完全清楚。
在这里,我们建议描述一种以前未知的细菌之间交流的途径
真核宿主及其在介导黏膜相关免疫调节作用中的作用
共生关系。为了确定流程的性质,我们将确定参与和需求的特征
通过化学和遗传方法相结合的多种内吞途径。我们还将
在一种新的体外系统中产生并检查这些相互作用。
如果成功,我们的研究将揭示一种新的运送细菌抗原的机制
肠道中共系膜特异性T细胞的激活和/或细菌分子的传递
免疫调节。
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:
$ 24万 - 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:
$ 24万 - 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:
$ 24万 - 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:
9902326 - 财政年份:2019
- 资助金额:
$ 24万 - 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:
$ 24万 - 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:
$ 24万 - 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:
$ 24万 - 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:
$ 24万 - 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:
$ 24万 - 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:
$ 24万 - 项目类别:
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