2021
Potential Implications of a Type 1 Interferon Gene Signature on COVID-19 Severity and Chronic Inflammation in Sickle Cell Disease
Madany E, Okwan-Duodu D, Balbuena-Merle R, Hendrickson JE, Gibb DR. Potential Implications of a Type 1 Interferon Gene Signature on COVID-19 Severity and Chronic Inflammation in Sickle Cell Disease. Frontiers In Medicine 2021, 8: 679030. PMID: 34368185, PMCID: PMC8339405, DOI: 10.3389/fmed.2021.679030.Peer-Reviewed Original ResearchSickle cell diseaseCOVID-19 severityIFNα/βType 1 interferonCell diseaseSARS-CoV-2 infectionType 1 interferon responseCorona Virus Disease-19 (COVID-19) pandemicCohort of patientsMajority of patientsInterferon gene signatureIFNα/β productionRace-matched controlsDisease-19 pandemicCOVID-19Express elevated levelsMajority of evidenceSCD diseaseSevere sequelaeChronic inflammationFavorable outcomeVariable progressionClinical consequencesGeneral populationPatientsThe lysophospholipid‐binding molecule CD1D is not required for the alloimmunization response to fresh or stored RBCs in mice despite RBC storage driving alterations in lysophospholipids
Medved J, Knott BM, Tarrah SN, Li AN, Shah N, Moscovich TC, Boscia AR, Salazar JE, Santhanakrishnan M, Hendrickson JE, Fu X, Zimring JC, Luckey CJ. The lysophospholipid‐binding molecule CD1D is not required for the alloimmunization response to fresh or stored RBCs in mice despite RBC storage driving alterations in lysophospholipids. Transfusion 2021, 61: 2169-2178. PMID: 34181769, PMCID: PMC8856511, DOI: 10.1111/trf.16554.Peer-Reviewed Original ResearchMeSH KeywordsAlarminsAnimalsAntibody SpecificityAntigens, CD1dBlood PreservationBlood TransfusionDuffy Blood-Group SystemErythrocytesFemaleImmunizationImmunoglobulin GImmunoglobulin MIsoantibodiesIsoantigensLysophospholipidsMaleMass SpectrometryMiceMice, Inbred StrainsMice, KnockoutMice, TransgenicMuramidaseOvalbuminReceptors, Cell SurfaceTransfusion ReactionConceptsCD1d-deficient miceCD1d deficiencyRBC alloimmunizationImmune activationNonclassical major histocompatibility complex class IWild-type control miceMajor histocompatibility complex class IHistocompatibility complex class IAdverse clinical consequencesSignificant adverse clinical consequencesLow baseline levelsRBC storageComplex class IHOD RBCsMolecule CD1dRBC transfusionWT miceControl miceImmune responseClinical consequencesMouse modelCD1dCD1d recognitionPolyclonal immunoglobulinsBaseline levels
2017
Interleukin-6 receptor α signaling on CD4+ T cells drives RBC alloantibody generation and T follicular helper cell differentiation in a murine model of RBC alloimmunization.
Arneja A, Salazar J, Jiang W, Hendrickson J, Zimring J, Luckey C. Interleukin-6 receptor α signaling on CD4+ T cells drives RBC alloantibody generation and T follicular helper cell differentiation in a murine model of RBC alloimmunization. The Journal Of Immunology 2017, 198: 201.27-201.27. DOI: 10.4049/jimmunol.198.supp.201.27.Peer-Reviewed Original ResearchRBC alloimmunizationRed blood cellsIL-6RαT cellsAntigen-negative red blood cellsFollicular helper cell differentiationInterleukin-6 receptor αFollicular helper cellsHemolytic transfusion reactionsViable therapeutic optionLife-saving therapySignificant clinical problemSignificant clinical consequencesInterleukin-6 receptorHelper cell differentiationSpecific CD4Multiple alloantibodiesOccasional mortalitySignificant morbidityTherapeutic optionsAvailable biologicsFunctional outcomeHelper cellsTransfusion reactionsClinical consequences