2021
Dectin-1 limits CNS autoimmunity through a non-canonical pathway
Deerhake M, Danzaki K, Inoue M, Cardakli E, Nonaka T, Aggarwal N, Barclay W, Ji R, Shinohara M. Dectin-1 limits CNS autoimmunity through a non-canonical pathway. The Journal Of Immunology 2021, 206: 96.07-96.07. DOI: 10.4049/jimmunol.206.supp.96.07.Peer-Reviewed Original ResearchExperimental autoimmune encephalomyelitisC-type lectin receptorsCentral nervous systemMultiple sclerosisInnate immunityDectin-1 pathwayCNS autoimmunityEAE severityAutoimmune encephalomyelitisNeuroprotective cytokineNeuroprotective functionNeurologic disordersPathologic roleImmune responseAnimal modelsNervous systemMyeloid cellsOSM receptorNon-canonical pathwayUpregulated expressionOncostatin MLectin receptorsAutoimmunityRNA-seq profilingProtective aspectsDectin-1 limits autoimmune neuroinflammation and promotes myeloid cell-astrocyte crosstalk via Card9-independent expression of Oncostatin M
Deerhake ME, Danzaki K, Inoue M, Cardakli ED, Nonaka T, Aggarwal N, Barclay WE, Ji RR, Shinohara ML. Dectin-1 limits autoimmune neuroinflammation and promotes myeloid cell-astrocyte crosstalk via Card9-independent expression of Oncostatin M. Immunity 2021, 54: 484-498.e8. PMID: 33581044, PMCID: PMC7956124, DOI: 10.1016/j.immuni.2021.01.004.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAstrocytesBrainCARD Signaling Adaptor ProteinsCell CommunicationCells, CulturedDisease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalGalectinsGene Expression RegulationLectins, C-TypeMice, Inbred C57BLMice, KnockoutMultiple SclerosisMyelin-Oligodendrocyte GlycoproteinMyeloid CellsNeurogenic InflammationOncostatin MOncostatin M Receptor beta SubunitPeptide FragmentsReceptors, MitogenSignal TransductionConceptsExperimental autoimmune encephalomyelitisC-type lectin receptorsCentral nervous systemAutoimmune neuroinflammationOncostatin MPro-resolution functionHeat-killed mycobacteriaDectin-1 pathwayDectin-1 ligandsPotential therapeutic targetEAE severityAutoimmune encephalomyelitisNeuroprotective moleculesNeurologic disordersPathologic roleGalectin-9Therapeutic targetTranscription factor NFATNervous systemMyeloid cellsInnate immunityOSM receptorLectin receptorsEnhanced gene expressionNeuroinflammation
2015
The Role of Stem Cells in the Etiology and Pathophysiology of Endometriosis
Hufnagel D, Li F, Cosar E, Krikun G, Taylor HS. The Role of Stem Cells in the Etiology and Pathophysiology of Endometriosis. Seminars In Reproductive Medicine 2015, 33: 333-340. PMID: 26375413, PMCID: PMC4986990, DOI: 10.1055/s-0035-1564609.Peer-Reviewed Original ResearchConceptsStem cellsStem cell populationProgenitor stem cellsStem cell traffickingCyclic regenerationPool of cellsCell mobilityBone marrow-derived stem cellsMarrow-derived stem cellsDynamic organRecent characterizationUnrestrained growthCell populationsCell traffickingEctopic sitesCellsRapid regenerationHuman endometriumRegenerationPathologic roleGrowthEndometriosis interferesPathophysiology of endometriosisDevelopment of endometriosisTrafficking
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