2025
A genetically modulated Toll-like receptor-tolerant phenotype in peripheral blood cells of children with multisystem inflammatory syndrome.
Khan R, Ji W, Guzman Rivera J, Madhvi A, Andrews T, Richlin B, Suarez C, Gaur S, Hasan U, Cuddy W, Singh A, Bukulmez H, Kaelber D, Kimura Y, Ganapathi U, Michailidis I, Ukey R, Moroso-Fela S, Kuster J, Casseus M, Roy J, Burns J, Kleinman L, Horton D, Lakhani S, Gennaro M. A genetically modulated Toll-like receptor-tolerant phenotype in peripheral blood cells of children with multisystem inflammatory syndrome. The Journal Of Immunology 2025, 214: 373-383. PMID: 40101747, PMCID: PMC11952872, DOI: 10.1093/jimmun/vkaf006.Peer-Reviewed Original ResearchToll-like receptorsLysosomal trafficking regulatorClinical laboratory indicatorsMIS-CMultisystem inflammatory syndromePeripheral blood cellsInflammatory syndromeLaboratory indicatorsHeterozygous carriersAgonists of Toll-like receptorsTLR responsesGut leakage markersDysregulated innate immune responseGenetic background of patientsBlood cells of childrenMIS-C patientsImmune response initiationIncreased Plasma LevelsNegative regulator of TLR signalingMIS-C childrenAssociated with hyperinflammationGenetic backgroundRegulator of TLR signalingBackground of patientsCells of children
2022
IFITM3 restricts virus-induced inflammatory cytokine production by limiting Nogo-B mediated TLR responses
Clement M, Forbester J, Marsden M, Sabberwal P, Sommerville M, Wellington D, Dimonte S, Clare S, Harcourt K, Yin Z, Nobre L, Antrobus R, Jin B, Chen M, Makvandi-Nejad S, Lindborg J, Strittmatter S, Weekes M, Stanton R, Dong T, Humphreys I. IFITM3 restricts virus-induced inflammatory cytokine production by limiting Nogo-B mediated TLR responses. Nature Communications 2022, 13: 5294. PMID: 36075894, PMCID: PMC9454482, DOI: 10.1038/s41467-022-32587-4.Peer-Reviewed Original ResearchConceptsInterferon-induced transmembrane protein 3IL-6 productionViral pathogenesisCytokine productionPro-inflammatory cytokine productionInflammatory cytokine productionInflammatory cytokine responseSARS-CoV-2Transmembrane protein 3Dendritic cellsCytokine responsesImmunoregulatory pathwaysImmunoregulatory functionsTLR2 responsesTLR responsesMouse modelMyeloid cellsViral stimulationProtein 3PathogenesisRestriction factorsNogoCellular localizationResponseCells
2014
An ENU-induced splicing mutation reveals a role for Unc93b1 in early immune cell activation following influenza A H1N1 infection
Lafferty EI, Flaczyk A, Angers I, Homer R, d'Hennezel E, Malo D, Piccirillo CA, Vidal SM, Qureshi ST. An ENU-induced splicing mutation reveals a role for Unc93b1 in early immune cell activation following influenza A H1N1 infection. Genes & Immunity 2014, 15: 320-332. PMID: 24848930, PMCID: PMC4978536, DOI: 10.1038/gene.2014.22.Peer-Reviewed Original ResearchMeSH KeywordsAlternative SplicingAnimalsCD8-Positive T-LymphocytesChemokine CXCL10EndosomesEthylnitrosoureaImmunity, InnateInfluenza A Virus, H1N1 SubtypeInterferon Type IInterferon-gammaL-SelectinLungLymphocyte ActivationMacrophage ActivationMembrane Transport ProteinsMiceMice, Inbred C57BLMutationOrthomyxoviridae InfectionsToll-Like ReceptorsConceptsEndosomal TLRsImmune responseEndosomal Toll-like receptorsInfluenza A/PR/8/34Expression of CXCL10Toll-like receptorsImmune cell activationCD69 activation markerInnate immune responseHuman infectious diseasesViral clearanceActivation markersInfected lungsRespiratory pathogensTLR responsesT cellsLymphoid cellsCell activationTissue pathologyInfectious diseasesMouse strainsInfectionExudate macrophagesReduced expressionUNC93B1
2008
The Influence of Injury on Toll-Like Receptor Responses
Murphy T, Maung A, Paterson H, Lederer J. The Influence of Injury on Toll-Like Receptor Responses. 2008, 185-202. DOI: 10.1201/9781420043198-17.ChaptersToll-like receptorsToll-like receptor responsesAdaptive immune responsesInfluence of injuryStrong inflammatory responseInnate immune systemCommon microbial antigensSentinel receptorsTLR ligandsMicrobial antigensInflammatory responseViral antigensTissue injuryTLR responsesImmune responseCell injuryReceptor responsesImmune systemTissue damageInjury responseEndogenous factorsMicrobial ligandsInjuryInfectionIntracellular receptors
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