Mechanisms by which M. tuberculosis 13KDa lectin modulates human immune responses
Mechanisms by which M. tuberculosis 13KDa lectin modulates human immune responses
批准号:
8311544
负责人:
Andre Bafica
金额:
$5.31万
依托单位国家:
美国
项目类别:
财政年份:
2009
资助国家:
美国
项目状态:
已结题
起止时间:
2009-09-01 至 2013-08-31
关键词:
AgonistAntibiotic TherapyAntigen-Presenting CellsAntitubercular AgentsBacteriaBindingBiochemicalBioinformaticsBiological MarkersBlocking AntibodiesBrazilC Type Lectin ReceptorsC-Type LectinsCD209 geneCD80 geneCell CommunicationCell Culture TechniquesCell LineCell physiologyCellsCitiesCoculture TechniquesCommunicable DiseasesConfocal MicroscopyCytokine GeneCytometryDataData AnalysesDatabasesDendritic CellsDevelopmentDiagnosticDiseaseEnzyme-Linked Immunosorbent AssayErythrocytesExposure toFamilyFlow CytometryGene ExpressionGenesGenus MycobacteriumGoalsGreen Fluorescent ProteinsHealthHost resistanceHumanImmune responseImmune systemImmunityImmunoglobulin GImmunologic ReceptorsImmunotherapyIn VitroInfectionInflammation MediatorsInflammatoryInterferon Type IIInterleukin-10Interleukin-12Interleukin-17Interleukin-6KnowledgeLectinLung diseasesMHC Class II GenesMacrophage-1 AntigenMeasuresMembraneModelingMonoclonal AntibodiesMusMycobacterium smegmatisMycobacterium tuberculosisOutcomeOutcome StudyPathogenesisPathway interactionsPatient MonitoringPatientsPatternPeripheral Blood Mononuclear CellPhagocytosisPlayPreparationProcessProductionProtein Binding DomainProteinsPublishingReagentRecombinantsResearchRicinRoleScreening procedureSerumSurfaceSystemT-Cell ProliferationT-LymphocyteTLR2 geneTLR3 geneTLR4 geneTLR7 geneTNF geneTNFRSF5 geneTestingTimeToll-like receptorsTuberculosisVirulenceWorkbasechemotherapycohortcytokinedectin 1glucan phosphateimmunoprophylaxisimprovedin vivointerestinterleukin-23laminaranmacrophagemonocytemycobacterialneutralizing antibodynovelpathogenprotein protein interactionreceptorreceptor expressionresearch studyresponsestemsugartooltuberculosis treatmentuptake
中文摘要
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英文摘要
Mechanisms by which M. tuberculosis 13 kDa lectin modulates human
immune responses
Project Summary
Study of novel proteins from Mycobacterium tuberculosis may be a critical step for
improving diagnostic tools, therapies and immunoprophylaxis against tuberculosis (TB),
one of the most prevalent infectious diseases wordwide. We have identified a 13 KDa
ricin-like lectin from M. tuberculosis that was found to agglutinate red blood cells and
induce cytokine expression by macrophages. Moreover, serum from active tuberculosis
patients contained high levels of IgG against this lectin. In the present proposal, we aim
to characterize the role of 13 KDa Mtb lectin on human immune responses. The specific
aims of the study are to 1) characterize the innate immune response profile elicited
by the 13 KDa Mtb lectin; 2) determine innate receptor(s) expressed on human
APC involved in the recognition of 13 KDa Mtb lectin; 3) investigate the role of 13
KDa Mtb lectin in the infection/phagocytosis process of M. tuberculosis by human
APC and 4) examine specific humoral and cellular immune responses against 13
KDa Mtb lectin in TB patients before and after antibiotic treatment. Our long-term
goal is to determine whether 13 KDa Mtb ricin-like lectin plays a role in regulating human
immune responses to TB focusing on it possible activity in controlling APC function.
These studies could be important in revealing a new target for immunotherapy of
tuberculosis.
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会议论文
Mechanisms by which M. tuberculosis 13KDa lectin modulates human immune responses
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批准号:7688816
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项目类别:
-
资助金额:$5.28万
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财政年份:2009
-
负责人:Andre Bafica
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依托单位:
Mechanisms by which M. tuberculosis 13KDa lectin modulates human immune responses
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批准号:7922655
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项目类别:
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资助金额:$5.17万
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财政年份:2009
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负责人:Andre Bafica
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依托单位:
Mechanisms by which M. tuberculosis 13KDa lectin modulates human immune responses
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批准号:8712591
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项目类别:
-
资助金额:$5.35万
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财政年份:2009
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负责人:Andre Bafica
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依托单位:
Mechanisms by which M. tuberculosis 13KDa lectin modulates human immune responses
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批准号:8508839
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项目类别:
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资助金额:$4.99万
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财政年份:2009
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负责人:Andre Bafica
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依托单位:
海外基金