2021
ARID1A Mutation May Define an Immunologically Active Subgroup in Patients with Microsatellite Stable Colorectal Cancer
Sarshekeh A, Alshenaifi J, Roszik J, Manyam G, Advani S, Katkhuda R, Verma A, Lam M, Willis J, Shen J, Morris J, Davis J, Loree J, Lee H, Ajani J, Maru D, Overman M, Kopetz S. ARID1A Mutation May Define an Immunologically Active Subgroup in Patients with Microsatellite Stable Colorectal Cancer. Clinical Cancer Research 2021, 27: 1663-1670. PMID: 33414133, PMCID: PMC7956157, DOI: 10.1158/1078-0432.ccr-20-2404.Peer-Reviewed Original ResearchConceptsMicrosatellite stable colorectal cancerColorectal cancerStable colorectal cancerMutant casesCancer Center databaseT-cell markersTumor mutational burdenAT-rich interactive domain 1AUnique molecular subgroupSignificant higher expressionCancer Genome AtlasImmunologic featuresIFNγ expressionImmune activationImmune subtypesTreatment strategiesPreclinical modelsT cellsImmune responseMutational burdenSeparate cohortPatientsTherapy trialsActive subgroupMolecular subgroups
2019
Severe Leptospirosis Features in the Spleen Indicate Cellular Immunosuppression Similar to That Found in Septic Shock
Duarte-Neto A, Croda J, Pagliari C, Soriano F, Nicodemo A, Duarte M. Severe Leptospirosis Features in the Spleen Indicate Cellular Immunosuppression Similar to That Found in Septic Shock. Frontiers In Immunology 2019, 10: 920. PMID: 31114579, PMCID: PMC6503108, DOI: 10.3389/fimmu.2019.00920.Peer-Reviewed Original ResearchConceptsSeptic shockLeptospirosis patientsSevere leptospirosisPulmonary hemorrhagePositive cellsRed pulpBacterial septic shockSeptic shock patientsCaspase-3-positive cellsImmune cell markersSpleen of patientsActive caspase-3 positive cellsSemi-quantitative scoreImmunomodulatory treatmentShock patientsCellular immunosuppressionIL-10Immunologic featuresImmunosuppressive stateMarked atrophyEndothelial activationControl spleensHistological featuresIntense infiltrationPlasma cells
2015
TNF receptor superfamily member 13b (TNFRSF13B) hemizygosity reveals transmembrane activator and CAML interactor haploinsufficiency at later stages of B-cell development
Romberg N, Virdee M, Chamberlain N, Oe T, Schickel JN, Perkins T, Cantaert T, Rachid R, Rosengren S, Palazzo R, Geha R, Cunningham-Rundles C, Meffre E. TNF receptor superfamily member 13b (TNFRSF13B) hemizygosity reveals transmembrane activator and CAML interactor haploinsufficiency at later stages of B-cell development. Journal Of Allergy And Clinical Immunology 2015, 136: 1315-1325. PMID: 26100089, PMCID: PMC4641026, DOI: 10.1016/j.jaci.2015.05.012.Peer-Reviewed Original ResearchMeSH KeywordsAdolescentAdultAgedAged, 80 and overAntibody FormationAutoimmunityB-LymphocytesChildCommon Variable ImmunodeficiencyFemaleHaploinsufficiencyHemizygoteHumansImmunologic MemoryLymphocyte ActivationMaleMiddle AgedMutation, MissenseSmith-Magenis SyndromeT-Lymphocytes, RegulatoryTransmembrane Activator and CAML Interactor ProteinYoung AdultConceptsCommon variable immune deficiencyMemory B cellsB cell toleranceB cellsSmith-Magenis syndromeTACI expressionTNFRSF13B mutationsTransmembrane activatorB cell developmentTNF receptorRegulatory T cell functionPeripheral B cell toleranceAntibody-deficient patientsCentral B cell toleranceVariable immune deficiencyT cell functionAutoreactive B cellsNaive B cellsReactivity of antibodiesB cell activationMissense mutationsSingle B cellsAutoimmune featuresImmunologic featuresImmune deficiency
1984
NIH conference. T-cell lymphoproliferative syndrome associated with human T-cell leukemia/lymphoma virus.
Broder S, Bunn P, Jaffe E, Blattner W, Gallo R, Wong-Staal F, Waldmann T, DeVita V. NIH conference. T-cell lymphoproliferative syndrome associated with human T-cell leukemia/lymphoma virus. Annals Of Internal Medicine 1984, 100: 543-57. PMID: 6322632, DOI: 10.7326/0003-4819-100-4-543.Peer-Reviewed Original ResearchMeSH KeywordsAcquired Immunodeficiency SyndromeAdultAnimalsCell Transformation, NeoplasticCell Transformation, ViralDeltaretrovirusFemaleHumansLeukemia, LymphoidLymph NodesLymphomaLymphoproliferative DisordersMaleMiddle AgedNeoplastic Cells, CirculatingPhenotypeSyndromeT-LymphocytesTumor Virus InfectionsConceptsHuman T-cell leukemia/lymphoma virusAdult T-cell leukemia/lymphomaT-cell leukemia/lymphomaT-cell tropicLeukemia/lymphomaImmunologic featuresOpportunistic infectionsLymphoproliferative disordersLymphoproliferative syndromeMolecular biologicRNA tumor virusesTumor virusVirusClasses of retrovirusesMajor advancesRetrovirusesHypercalcemia
1983
The Spirochetal Etiology of Lyme Disease
Steere A, Grodzicki R, Kornblatt A, Craft J, Barbour A, Burgdorfer W, Schmid G, Johnson E, Malawista S. The Spirochetal Etiology of Lyme Disease. New England Journal Of Medicine 1983, 308: 733-740. PMID: 6828118, DOI: 10.1056/nejm198303313081301.Peer-Reviewed Original ResearchConceptsLyme diseaseAntibody titersIgM titersSpecific IgM antibody titersSpecific IgG antibody titersElevated IgM titersI. dammini spirocheteIgG antibody titersIgM antibody titersTiters of IgGOnset of diseaseInfectious mononucleosisControl patientsImmunologic featuresIgG titersEarly diseaseControl subjectsSpirochetal etiologySkin lesionsCerebrospinal fluidPatientsLate manifestationSixth weekDiseaseTiters
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