Wesley Tung
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Research
Publications
2021
Inborn errors of TLR3- or MDA5-dependent type I IFN immunity in children with enterovirus rhombencephalitis
Chen J, Jing H, Martin-Nalda A, Bastard P, Rivière J, Liu Z, Colobran R, Lee D, Tung W, Manry J, Hasek M, Boucherit S, Lorenzo L, Rozenberg F, Aubart M, Abel L, Su H, Palacin P, Casanova J, Zhang S. Inborn errors of TLR3- or MDA5-dependent type I IFN immunity in children with enterovirus rhombencephalitis. Journal Of Experimental Medicine 2021, 218: e20211349. PMID: 34726731, PMCID: PMC8570298, DOI: 10.1084/jem.20211349.Peer-Reviewed Original ResearchMeSH KeywordsCells, CulturedChild, PreschoolEncephalitis, ViralEnterovirusEnterovirus InfectionsFemaleFibroblastsHumansInfantInterferon alpha-2Interferon-betaInterferon-Induced Helicase, IFIH1Loss of Function MutationMaleMetabolism, Inborn ErrorsPoly I-CRhombencephalonToll-Like Receptor 3Virus ReplicationConceptsIFN-α2bVirus-induced type I IFN productionType I IFN productionLife-threatening infectionsI IFN productionCentral nervous systemPost-infection treatmentCell-intrinsic immunityLater time pointsEnterovirus infectionHuman TLR3IFN productionNervous systemTLR3Unrelated childrenViral phenotypeInborn errorsViral susceptibilityTime pointsIFIH1 variantsInfectionRhombencephalitisCell linesEV30MDA5IFIH1 loss-of-function variants contribute to very early-onset inflammatory bowel disease
Cananzi M, Wohler E, Marzollo A, Colavito D, You J, Jing H, Bresolin S, Gaio P, Martin R, Mescoli C, Bade S, Posey J, Dalle Carbonare M, Tung W, Jhangiani S, Bosa L, Zhang Y, Filho J, Gabelli M, Kellermayer R, Kader H, Oliva-Hemker M, Perilongo G, Lupski J, Biffi A, Valle D, Leon A, de Macena Sobreira N, Su H, Guerrerio A. IFIH1 loss-of-function variants contribute to very early-onset inflammatory bowel disease. Human Genetics 2021, 140: 1299-1312. PMID: 34185153, PMCID: PMC8423350, DOI: 10.1007/s00439-021-02300-4.Peer-Reviewed Original ResearchConceptsInflammatory bowel diseaseOnset inflammatory bowel diseaseWhole-exome sequencingBowel diseaseMultiple infectious episodesHomozygous truncating variantViral nucleic acidsKey cytosolic sensorsLuciferase reporter assaysMDA5 activityInfectious episodesIBD pathogenesisVEOIBDGut homeostasisViral sensitivityIndependent cohortInnate immunityHypomorphic variantsTruncating variantsImmunological issuesViral sensingIFIH1 geneFunction variantsCytosolic sensorsExome sequencing
2020
IMMU-25. SEVERE AND MULTIFACETED SYSTEMIC IMMUNOSUPPRESSION CAUSED BY EXPERIMENTAL CANCERS OF THE CENTRAL NERVOUS SYSTEM REQUIRES RELEASE OF NON-STEROID SOLUBLE MEDIATORS
Ayasoufi K, Pfaller C, Evgin L, Khadka R, Tritz Z, Goddery E, Fain C, Yokanovich L, Himes B, Jin F, Zheng J, Schuelke M, Hansen M, Tung W, Parney I, Pease L, Vile R, Johnson A. IMMU-25. SEVERE AND MULTIFACETED SYSTEMIC IMMUNOSUPPRESSION CAUSED BY EXPERIMENTAL CANCERS OF THE CENTRAL NERVOUS SYSTEM REQUIRES RELEASE OF NON-STEROID SOLUBLE MEDIATORS. Neuro-Oncology 2020, 22: ii110-ii110. PMCID: PMC7650917, DOI: 10.1093/neuonc/noaa215.455.Peer-Reviewed Original ResearchT-cell countsCD4 T-cell countMHC class II expressionDiffuse intrinsic pontine gliomaClass II expressionThymic involutionT cellsCell countLow CD4 T-cell countsMHC class II expression levelPeripheral T-cell countsSignificant thymic involutionT cell sequestrationAcute neurological insultsCD4 T cellsHallmark featurePeripheral blood monocytesPeripheral T cellsNeurological disease modelsBlood-derived factorsIntrinsic pontine gliomaSystemic immunosuppressionGL261 gliomasBrain insultsCNS cancers
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