RNA binding proteins in end-organ autoimmune pathology
终末器官自身免疫病理学中的 RNA 结合蛋白
基本信息
- 批准号:10569112
- 负责人:
- 金额:$ 64.36万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2022
- 资助国家:美国
- 起止时间:2022-02-08 至 2027-01-31
- 项目状态:未结题
- 来源:
- 关键词:Anti-Glomerular Basement Membrane DiseaseAntibodiesAntigen TargetingAntineutrophil Cytoplasmic AntibodiesAutoantibodiesAutoimmuneAutoimmune DiseasesAutoimmunityAutomobile DrivingBindingBiologicalBiological MarkersBiological Response ModifiersBiopsyBlood VesselsCCAAT-Enhancer-Binding ProteinsCCAAT-enhancer-binding protein-deltaCellsComplexCytokine SignalingDataDepositionDiseaseDrug TargetingElementsEpithelial CellsEquilibriumEventGene ExpressionGenerationsGenesGlomerulonephritisGoalsGoodpasture SyndromeHalf-LifeHelper-Inducer T-LymphocyteHumanIL17 geneImageImmune systemImmunologyImpairmentInflammationInterleukin-6KidneyKidney DiseasesLCN2 geneMediatingMessenger RNAModificationMolecularMolecular TargetMusNeutrophil InfiltrationOrganPathogenesisPathogenicityPathologicPathologyPathway interactionsPatientsPhysiologicalPost-Transcriptional RegulationProcessPublishingRNARNA-Binding ProteinsRegulationResistanceRoleSignal TransductionTissuesTranslationsTubular formationUp-RegulationVasculitisautoinflammationautoinflammatorycell typechemokinecytokineimprovedin vivokidney biopsykidney cellmicroorganismmouse modelmurine antibodynovelpathogenposttranscriptionalrenal damagesuccesstargeted treatmenttranscription factor
项目摘要
IL-17 and Th17 cells are dysregulated in many pathologic auto-inflammatory conditions.
Antibody-mediated glomerulonephritis (AGN) occurs when unchecked inflammation triggered by
autoimmune Ab complexes that deposit in glomeruli and lead to kidney damage, which occurs in
conditions such as Goodpasture disease, ANCA vasculitis, etc. Although the initiators of
autoantibody-mediated pathology differ, the terminal events in end organ kidney damage have
many common hallmarks, and the fundamental immunology of this process is still not well
understood. Accumulating evidence from our groups and others have convincingly demonstrated
role for IL-17 in driving pathogenesis of AGN in humans and in mouse models. Excessive
autoimmune pathology can be caused by hyper-production of cytokines from T helper cells or by
over-exuberant cytokine signaling. Therefore, in principle, molecules that influence IL-17 signal
transduction have the potential to be viable targets for therapy in settings where this cytokine is a
disease driver. In probing the fundamental mechanisms that mediate IL-17-dependent signaling,
we identified two novel RNA binding proteins (RBPs) that contribute significantly to the
pathogenesis of AGN in vivo. These RBPs are downstream of IL-17 and their activities in the IL-
17 pathway are interconnected through regulation of CCAAT Enhancer Binding Protein (C/EBP)
transcription factors. In turn, C/EBPs mediate IL-17-dependent effectors that promote renal
inflammation, including Lipocalin-2, neutrophil-recruiting chemokines, and feed-forward activators
of Th17 differentiation such as IL-6. Our central hypothesis is that IL-17 promotes inflammation
through post-transcriptional regulation of downstream mRNAs that drive renal pathology in AGN.
This proposal will evaluate the molecular mechanisms by which these RBPs act and the specific
physiological functions in the setting of AGN.
IL-17和Th17细胞在许多病理性自身炎症条件下失调。
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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Partha Sarathi Biswas其他文献
Correction: Genomic prediction and QTL analysis for grain Zn content and yield in Aus-derived rice populations
- DOI:
10.1007/s13562-025-00983-8 - 发表时间:
2025-04-28 - 期刊:
- 影响因子:1.500
- 作者:
Tapas Kumer Hore;C. H. Balachiranjeevi;Mary Ann Inabangan-Asilo;C. A. Deepak;Alvin D. Palanog;Jose E. Hernandez;Glenn B. Gregorio;Teresita U. Dalisay;Maria Genaleen Q. Diaz;Roberto Fritsche Neto;Md. Abdul Kader;Partha Sarathi Biswas;B. P. Mallikarjuna Swamy - 通讯作者:
B. P. Mallikarjuna Swamy
Partha Sarathi Biswas的其他文献
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{{ truncateString('Partha Sarathi Biswas', 18)}}的其他基金
RNA binding proteins in end-organ autoimmune pathology
终末器官自身免疫病理学中的 RNA 结合蛋白
- 批准号:
10450945 - 财政年份:2022
- 资助金额:
$ 64.36万 - 项目类别:
Mechanisms of renal protection against disseminated candidiasis
抵抗播散性念珠菌病的肾脏保护机制
- 批准号:
10376250 - 财政年份:2021
- 资助金额:
$ 64.36万 - 项目类别:
Mechanisms of renal protection against disseminated candidiasis
抵抗播散性念珠菌病的肾脏保护机制
- 批准号:
10190010 - 财政年份:2021
- 资助金额:
$ 64.36万 - 项目类别:
Mechanisms of neutrophil dysfunction in antifungal immunity
中性粒细胞功能障碍在抗真菌免疫中的机制
- 批准号:
10454893 - 财政年份:2019
- 资助金额:
$ 64.36万 - 项目类别:
Mechanisms of neutrophil dysfunction in antifungal immunity
中性粒细胞功能障碍在抗真菌免疫中的机制
- 批准号:
9815169 - 财政年份:2019
- 资助金额:
$ 64.36万 - 项目类别:
Mechanisms of neutrophil dysfunction in antifungal immunity
中性粒细胞功能障碍在抗真菌免疫中的机制
- 批准号:
10223106 - 财政年份:2019
- 资助金额:
$ 64.36万 - 项目类别:
Mechanisms of neutrophil dysfunction in antifungal immunity
中性粒细胞功能障碍在抗真菌免疫中的机制
- 批准号:
10673766 - 财政年份:2019
- 资助金额:
$ 64.36万 - 项目类别:
Regulation of IL-17 signaling by RNA binding proteins in kidney diseases
RNA 结合蛋白在肾脏疾病中调节 IL-17 信号传导
- 批准号:
9762270 - 财政年份:2019
- 资助金额:
$ 64.36万 - 项目类别:
Mechanisms of IL-17 Mediated Host Defense in the Kidney
IL-17 介导的肾脏宿主防御机制
- 批准号:
9023669 - 财政年份:2015
- 资助金额:
$ 64.36万 - 项目类别:
Mechanisms of IL-17 Mediated Host Defense in the Kidney
IL-17 介导的肾脏宿主防御机制
- 批准号:
9144776 - 财政年份:2015
- 资助金额:
$ 64.36万 - 项目类别:
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