2022
The AIM2 inflammasome is activated in astrocytes during the late phase of EAE
Barclay WE, Aggarwal N, Deerhake ME, Inoue M, Nonaka T, Nozaki K, Luzum NA, Miao EA, Shinohara ML. The AIM2 inflammasome is activated in astrocytes during the late phase of EAE. JCI Insight 2022, 7: e155563. PMID: 35451371, PMCID: PMC9089781, DOI: 10.1172/jci.insight.155563.Peer-Reviewed Original ResearchConceptsExperimental autoimmune encephalomyelitisCentral nervous systemInflammasome activationInflammasome-mediated inflammationRole of inflammasomesApoptosis-associated speck-like proteinIL-1β releaseAIM2 inflammasome activationSpeck-like proteinAutoimmune encephalomyelitisEffector cytokinesAutoimmune conditionsIL-18Multiple sclerosisIL-1βDisease peakInflammatory responseSpinal cordMelanoma 2Mouse modelAnimal modelsReporter miceNervous systemMyeloid cellsAIM2 inflammasome
2021
Emerging roles of Dectin-1 in noninfectious settings and in the CNS
Deerhake ME, Shinohara ML. Emerging roles of Dectin-1 in noninfectious settings and in the CNS. Trends In Immunology 2021, 42: 891-903. PMID: 34489167, PMCID: PMC8487984, DOI: 10.1016/j.it.2021.08.005.Peer-Reviewed Original ResearchConceptsC-type lectin receptorsImmune responseProinflammatory immune responseCentral nervous systemNew therapeutic approachesInnate immune responseMammalian myeloid cellsNeuroprotective responseSterile inflammationNeurologic disordersTherapeutic approachesNervous systemMyeloid cellsFungal infectionsLectin receptorsRecent studiesCurrent understandingResponseInflammationΒ-glucanInfectionSettingImmunologyReceptorsDectin-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