2025
SARS-CoV-2 induced immune perturbations in infants vary with disease severity and differ from adults’ responses
Nehar-Belaid D, Mejías A, Xu Z, Marches R, Yerrabelli R, Chen G, Mertz S, Ye F, Sánchez P, Tsang J, Aydillo T, Miorin L, Cupic A, García-Sastre A, Ucar D, Banchereau J, Pascual V, Ramilo O. SARS-CoV-2 induced immune perturbations in infants vary with disease severity and differ from adults’ responses. Nature Communications 2025, 16: 4562. PMID: 40379618, PMCID: PMC12084365, DOI: 10.1038/s41467-025-59411-z.Peer-Reviewed Original ResearchConceptsResponse to SARS-CoV-2Infected infantsT cellsSARS-CoV-2B cellsCytotoxic CD8+ T cellsImmune profile of childrenISG signatureNaive CD4+ T cellsCD8+ T cellsCD4+ T cellsImmune response to SARS-CoV-2Anti-IFN autoantibodiesAntibody response to SARS-CoV-2Transitional B cellsEarly life immunityCD14+ monocytesIncreased serum concentrationsInflammasome-related moleculesInterferon-stimulated genesImmune profileImmune perturbationsSerum concentrationsInflammatory cytokinesImmune responseIdentification of Distinct Biological Groups of Patients With Cryptogenic NORSE via Inflammatory Profiling
Guillemaud M, Chavez M, Kobeissy F, Vezzani A, Jimenez A, Basha M, Batra A, Demeret S, Eka O, Eschbach K, Foreman B, Gaspard N, Gerard E, Gofton T, Haider H, Hantus S, Howe C, Jongeling A, Kalkach-Aparicio M, Kandula P, Kazazian K, Kim M, Lai Y, Marois C, Mellor A, Mohamed W, Morales M, Pimentel C, Ramirez A, Steriade C, Struck A, Taraschenko O, Torcida Sedano N, Wainwright M, Yoo J, Wang K, Navarro V, Hirsch L, Hanin A. Identification of Distinct Biological Groups of Patients With Cryptogenic NORSE via Inflammatory Profiling. Neurology Neuroimmunology & Neuroinflammation 2025, 12: e200403. PMID: 40334176, PMCID: PMC12063244, DOI: 10.1212/nxi.0000000000200403.Peer-Reviewed Original ResearchConceptsCryptogenic new-onset refractory status epilepticusClusters of patientsCytokine profileInflammatory markersNew-onset refractory status epilepticusTarget specific inflammatory pathwaysInitiation of immunotherapyResponse to immunotherapyRefractory status epilepticusPersonalized therapeutic strategiesGroup of patientsStatistically significant elevationTime of administrationProtein pathway analysisInflammatory subgroupsMultiple immunotherapiesDifferential treatment responseRefractory SEC patientsImprove patient outcomesAutoimmune mechanismsImmune dysregulationClinical featuresCytokine levelsAutoimmune processCD1d‐iNKT Axis in Infectious Diseases: Lessons Learned From the Past
Chatterjee P, Brahma S, Cresswell P, Bandyopadhyay S. CD1d‐iNKT Axis in Infectious Diseases: Lessons Learned From the Past. Scandinavian Journal Of Immunology 2025, 101: e70024. PMID: 40243400, DOI: 10.1111/sji.70024.Peer-Reviewed Original ResearchConceptsINKT cellsLipid antigensDiverse array of cytokinesRecognition of lipid antigensEra of immunotherapyINKT cell responsesInnate-like propertiesAntigen-presenting moleculesArray of cytokinesInfectious diseasesImmunotherapeutic strategiesBridge innateT lymphocytesAdjunctive therapyIFN-gIL-13IL-4Antimicrobial treatmentArray of lipidsInfluence immune reactionsAdaptive immunityImmune responseCases of infectious diseasesImmune reactionsGlycolipid antigensSkin damage signals mediate allergic sensitization to spatially unlinked antigen
Waizman D, Brown-Soler I, Martin A, Ma Y, Zhou K, Israni-Winger K, Zhang C, Medzhitov R, Launay P, Michieletto M, Henao-Mejia J, Palm N, Craft J, Eisenstein A, Wang A. Skin damage signals mediate allergic sensitization to spatially unlinked antigen. Science Immunology 2025, 10: eadn0688. PMID: 40184440, PMCID: PMC12100540, DOI: 10.1126/sciimmunol.adn0688.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigensCytokinesFemaleHypersensitivityImmunologic MemoryMiceMice, Inbred C57BLSkinActivation of macrophages by extracellular vesicles derived from Babesia-infected red blood cells
Hagos B, Brasov I, Branscome H, Rashid S, Bradford R, Leonelli J, Kashanchi F, Mamoun C, Molestina R. Activation of macrophages by extracellular vesicles derived from Babesia-infected red blood cells. Infection And Immunity 2025, 93: e00333-24. PMID: 40172538, PMCID: PMC12070731, DOI: 10.1128/iai.00333-24.Peer-Reviewed Original ResearchConceptsInfected red blood cellsPrimary cause of human babesiosisRed blood cellsExtracellular vesiclesActivated macrophagesResponse to <i>B.Host-pathogen interactionsModulation of pro-inflammatory cytokinesBlood cellsElimination of parasitesPro-inflammatory cytokinesActivation of NF-kBActivation of macrophagesRelease of extracellular vesiclesInnate immune responseIncubation of macrophagesUninfected RBCsCo-culture experimentsHuman babesiosisProtozoan parasitesCytokine secretionImmune responseMacrophage activationBabesiosisEV fractionsABO blood group and COVID-19 severity: Associations with endothelial and adipocyte activation in critically ill patients
Stukas S, Goshua G, Conway E, Lee A, Hoiland R, Sekhon M, Chen L. ABO blood group and COVID-19 severity: Associations with endothelial and adipocyte activation in critically ill patients. PLOS ONE 2025, 20: e0320251. PMID: 40173171, PMCID: PMC11964209, DOI: 10.1371/journal.pone.0320251.Peer-Reviewed Original ResearchConceptsABO blood groupCritically ill patientsIntensive care unitAB blood typeBlood groupEndothelial injuryInflammatory cytokinesLength of intensive care unitRetrospective single-center studyMarkers of endothelial activationIll patientsMarkers of endothelial injuryDays of ICU staySerum inflammatory markersSingle-center studySeverity of COVID-19 infectionSerum inflammatory cytokinesBlood typeVancouver General HospitalSevere COVID-19SARS-CoV-2 infectionSeverity of diseaseCOVID-19 severityAdipsin levelsEndothelial activationA Phase I, First-in-Human, Dose-Escalation, Expansion Trial of Cytokine-Encoding Synthetic mRNA Mixture Alone or with Cemiplimab in Advanced Solid Tumors
Bechter O, Loquai C, Champiat S, Baurain J, Grob J, Utikal J, Rottey S, Berrocal A, Hassel J, Arance A, Sanmamed M, Boers-Sonderen M, Gastman B, Gebhardt C, Delafontaine B, Sahin U, Türeci Ö, Brueck P, Abbadessa G, Marpadga R, Lee H, Yang Y, Buday B, Di Genova G, Wang H, Xia B, Lee J, Lebbe C. A Phase I, First-in-Human, Dose-Escalation, Expansion Trial of Cytokine-Encoding Synthetic mRNA Mixture Alone or with Cemiplimab in Advanced Solid Tumors. Clinical Cancer Research 2025, 31: 2358-2369. PMID: 40152791, PMCID: PMC12163594, DOI: 10.1158/1078-0432.ccr-24-1983.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overAntibodies, Monoclonal, HumanizedAntineoplastic Combined Chemotherapy ProtocolsCytokinesFemaleGranulocyte-Macrophage Colony-Stimulating FactorHumansInterferon alpha-2Interleukin-12Interleukin-15MaleMaximum Tolerated DoseMiddle AgedNeoplasmsRNA, MessengerTreatment OutcomeConceptsAdvanced solid tumorsMaximum administered doseSolid tumorsCombination therapyEscalation phaseTreated with anti-PD-1 therapyTreated with anticancer therapyAnti-PD-1 therapyTreatment-related adverse eventsDose level 8Predefined dose levelsInjection-site painFirst-in-humanPlasma cytokine concentrationsDose escalationAntitumor responsePartial responseIntratumoral administrationExpansion trialIL-15IFN-gCemiplimabAdverse eventsCytokine concentrationsDose levelsDecreased T helper 1 cell function underlies recurrent sinopulmonary infections in the 17q12 deletion syndrome
Shin J, Shin H, Gutierrez A, Yoo N, Par-Young J, Osmani L, Shin M, Sanchez-Lara P, Bucala R, Soffer G, Kang I. Decreased T helper 1 cell function underlies recurrent sinopulmonary infections in the 17q12 deletion syndrome. EBioMedicine 2025, 112: 105578. PMID: 39891996, PMCID: PMC11840234, DOI: 10.1016/j.ebiom.2025.105578.Peer-Reviewed Original ResearchConceptsCD4<sup>+</sup> T cellsRecurrent sinopulmonary infectionsT cell functionRNA-seq analysisT cellsHealthy controlsSinopulmonary infectionsRNA-seqT-betIFN-gFrequency of CD4<sup>+</sup> T cellsCD4<sup>+</sup> T cell functionTh1 transcription factor T-betDeletion syndromeFlow cytometryCompared to age-matched healthy controlsTranscription factor T-betDecreased T-betUrinary tract abnormalitiesAge-matched healthy controlsMultiplex assayDownstream effector cytokinesEffector cytokinesRecurrent infectionsTh17 cytokinesType 2 immunity to the rescue: enhancing antitumor immunity for skin cancer prevention
Vesely M, Christensen S. Type 2 immunity to the rescue: enhancing antitumor immunity for skin cancer prevention. Journal Of Clinical Investigation 2025, 135: e188018. PMID: 39744952, PMCID: PMC11684797, DOI: 10.1172/jci188018.Peer-Reviewed Original ResearchConceptsCutaneous squamous cell carcinomaThymic stromal lymphopoietinType 2 immunityActinic keratosisAK lesionsTh2 cellsPrevent cutaneous squamous cell carcinomaRecruitment of Th2 cellsCSCC preventionSquamous cell carcinomaMouse model of skin carcinogenesisModel of skin carcinogenesisDamage-associated molecular patternsKeratinocyte cell deathAntitumor immunityTopical calcipotriolSkin cancer preventionCell carcinomaPaired biopsiesPrecursor lesionsSkin carcinogenesisUnaffected skinMouse modelCancer preventionPremalignant keratinocytes
2024
Role of Toll-like receptor 2 during infection of Leptospira spp: A systematic review
Kappagoda C, Senavirathna I, Agampodi T, Agampodi S. Role of Toll-like receptor 2 during infection of Leptospira spp: A systematic review. PLOS ONE 2024, 19: e0312466. PMID: 39729468, PMCID: PMC11676585, DOI: 10.1371/journal.pone.0312466.Peer-Reviewed Original ResearchConceptsToll-like receptor 2Toll-like receptor 2 expressionReceptor 2TLR2 responsesSystematic reviewIn vivoImmune effectorsIn vitroEx vivoHuman studiesInvolvement of Toll-like receptor 2Systematic Review Centre for Laboratory Animal Experimentation riskInvolvement of TLR4Increased TLR2 expressionNational Institutes of Health Quality Assessment ToolEffective immune responseIn vitro studiesHuman leptospirosisTLR2 involvementRisk of biasIn vivo studiesTLR2 expressionOffice of Health AssessmentWeb of ScienceImmune responseDiverse NKT cells regulate early inflammation and neurological outcomes after cardiac arrest and resuscitation
Tamura T, Cheng C, Villaseñor-Altamirano A, Yamada K, Ikeda K, Hayashida K, Menon J, Chen X, Chung H, Varon J, Chen J, Choi J, Cullen A, Guo J, Lin X, Olenchock B, Pinilla-Vera M, Manandhar R, Sheikh M, Hou P, Lawler P, Oldham W, Seethala R, Baron R, Bohula E, Morrow D, Blumberg R, Chen F, Merriam L, Weissman A, Brenner M, Chen X, Ichinose F, Kim E, Sohn H, Rolland T, Weil B. Diverse NKT cells regulate early inflammation and neurological outcomes after cardiac arrest and resuscitation. Science Translational Medicine 2024, 16: eadq5796. PMID: 39630883, PMCID: PMC11792709, DOI: 10.1126/scitranslmed.adq5796.Peer-Reviewed Original ResearchConceptsOut-of-hospital cardiac arrestCohort of patientsNeurological outcomeT cellsImmune cellsCardiac arrestNatural killer (NK) cellsAssociated with good neurological outcomesDiverse T cell receptor repertoireNeurological injuryT cell receptor repertoireAssociated with poor neurological outcomeIncreased inflammatory chemokineInnate T cellsPoor neurological outcomeWild-type micePost-cardiac arrestAccumulation of macrophagesIncreased neuronal injuryBrains of miceNKT cellsTreated miceReceptor repertoireInflammatory chemokinesCytokine expressionKLF13 promotes SLE pathogenesis by modifying chromatin accessibility of key proinflammatory cytokine genes
Wang A, Fairhurst A, Liu K, Wakeland B, Barnes S, Malladi V, Viswanathan K, Arana C, Dozmorov I, Singhar A, Du Y, Imam M, Moses A, Chen C, Sunkavalli A, Casco J, Rakheja D, Li Q, Mohan C, Clayberger C, Wakeland E, Khan S. KLF13 promotes SLE pathogenesis by modifying chromatin accessibility of key proinflammatory cytokine genes. Communications Biology 2024, 7: 1446. PMID: 39506084, PMCID: PMC11541912, DOI: 10.1038/s42003-024-07099-0.Peer-Reviewed Original ResearchConceptsSystemic lupus erythematosusMyeloid cellsLupus nephritisT cellsKidneys of lupus-prone miceSystemic lupus erythematosus pathogenesisLevels of proinflammatory cytokinesLupus-prone miceActivated myeloid cellsActivated T cellsT cell activationProduction of RANTEST cell hyperactivityProinflammatory cytokine genesAssociated with increased productionLupus pathogenesisProinflammatory cytokines/chemokinesSle1 locusLupus erythematosusImmune activationProinflammatory cytokinesCytokine signaling pathwaysCytokine genesGenome-wide transcriptional changesReceptor ligandsGastrodenol suppresses NLRP3/GSDMD mediated pyroptosis and ameliorates inflammatory diseases
Chen P, Wang Y, Tang H, Liu Z, Wang J, Wang T, Xu Y, Ji S. Gastrodenol suppresses NLRP3/GSDMD mediated pyroptosis and ameliorates inflammatory diseases. Cellular Immunology 2024, 405: 104888. PMID: 39486308, DOI: 10.1016/j.cellimm.2024.104888.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCytokinesEncephalomyelitis, Autoimmune, ExperimentalFemaleGasderminsHumansInflammasomesInflammationIntracellular Signaling Peptides and ProteinsLipopolysaccharidesMacrophagesMiceMice, Inbred C57BLNLR Family, Pyrin Domain-Containing 3 ProteinPeritonitisPhosphate-Binding ProteinsPyroptosisConceptsNucleotide-binding oligomerization domain-like receptor family pyrin domain-containing protein 3Caspase activationRecruitment domainNLRP3 oligomerizationPyrin domain-containing protein 3Gasdermin D (GSDMD)-mediated pyroptosisProtein 3PyroptosisSecretion of pro-inflammatory cytokinesOligomerizationHydrogen bondsApoptosis-associated speck like proteinInflammatory diseasesTherapeutic strategiesHelicobacter pyloriPro-inflammatory cytokinesCaspaseExperimental autoimmune encephalomyelitisLipopolysaccharide (LPS)-inducedProteinGasderminInterleukin‐5 as a pleiotropic cytokine orchestrating airway type 2 inflammation: Effects on and beyond eosinophils
Buchheit K, Shaw D, Chupp G, Lehtimaki L, Heffler E, Finney‐Hayward T, Zangrilli J, Kwiatek J, Siddiqui S, Roufosse F, Thamboo A, West N, Vichiendilokkul A, Hellings P, Peters A, Howarth P. Interleukin‐5 as a pleiotropic cytokine orchestrating airway type 2 inflammation: Effects on and beyond eosinophils. Allergy 2024, 79: 2662-2679. PMID: 39359069, DOI: 10.1111/all.16303.Peer-Reviewed Original ResearchConceptsAnti-IL-5 therapyType 2 inflammationIL-5Airway type 2 inflammationT regulatory cellsInnate lymphoid cellsInterleukin (IL)-5Relevant to disease pathogenesisSurvival of eosinophilsLower airway diseaseEosinophil-associated diseasesEffector cellsEosinophil depletionTargeted therapyClinical benefitLymphoid cellsPlasma cellsAirway diseaseInterleukin-5Epithelial cellsTherapeutic effectMast cellsDisease pathogenesisEosinophilsTissue damageHuman induced pluripotent stem cell-derived cardiomyocytes to study inflammation-induced aberrant calcium transient
Tatekoshi Y, Chen C, Shapiro J, Chang H, Blancard M, Lyra-Leite D, Burridge P, Feinstein M, D'Aquila R, Hsue P, Ardehali H. Human induced pluripotent stem cell-derived cardiomyocytes to study inflammation-induced aberrant calcium transient. ELife 2024, 13: rp95867. PMID: 39331464, PMCID: PMC11434618, DOI: 10.7554/elife.95867.Peer-Reviewed Original ResearchConceptsHuman induced pluripotent stem cell-derived cardiomyocytesPluripotent stem cell-derived cardiomyocytesStem cell-derived cardiomyocytesCell-derived cardiomyocytesUptake in vitroHIV viremiaDiastolic dysfunctionHIV patientsCardiomyocyte relaxationSarcoplasmic reticulumSGLT2 inhibitorsHeart failurePotential new interventionsInflammatory cytokinesAnimal modelsHFpEFStudy molecular mechanismsMito-TEMPOCardiomyocytesCytokinesHIVPatientsRelaxation defectsPLWHSerumComparative Analysis of Viral Load and Cytokines during SARS-CoV-2 Infection between Pregnant and Non-Pregnant Women
Liu D, Li H, Li X, Rodriguez G, Pietz H, Fiel R, Konadu E, Singh V, Loo F, Rodgers W. Comparative Analysis of Viral Load and Cytokines during SARS-CoV-2 Infection between Pregnant and Non-Pregnant Women. International Journal Of Molecular Sciences 2024, 25: 7731. PMID: 39062978, PMCID: PMC11277191, DOI: 10.3390/ijms25147731.Peer-Reviewed Original ResearchConceptsNon-pregnant womenSARS-CoV-2 infectionResponse to SARS-CoV-2 infectionPregnant womenViral loadNeutralizing antibodiesImmune response to SARS-CoV-2 infectionAnalysis of viral loadSARS-CoV-2Retrospective cohort studyIgG neutralizing antibodiesCytokine expression patternsMultiplex reverse transcription polymerase chain reactionAnti-N protein IgGExpression of leptinDifferential cytokine expressionEnhanced antibody productionReverse transcription polymerase chain reactionVulnerability of pregnant womenCytokine array assayTranscription polymerase chain reactionCytokine profileIncidence of SARS-CoV-2 infectionImmune modulationPolymerase chain reactionHigh burden of viruses and bacterial pathobionts drives heightened nasal innate immunity in children
Watkins T, Green A, Amat J, Cheemarla N, Hänsel K, Lozano R, Dudgeon S, Germain G, Landry M, Schulz W, Foxman E. High burden of viruses and bacterial pathobionts drives heightened nasal innate immunity in children. Journal Of Experimental Medicine 2024, 221: e20230911. PMID: 38949638, PMCID: PMC11215523, DOI: 10.1084/jem.20230911.Peer-Reviewed Original ResearchConceptsBacterial pathobiontsRespiratory virusesBurden of virusesSARS-CoV-2Innate immune activationSARS-CoV-2 viral loadDynamic host-pathogen interactionsInnate immune responseViral coinfectionCytokine profileViral loadNasal virusImmune activationProinflammatory responseIL-1BNasopharyngeal samplesHost-pathogen interactionsImmune responseInterferon responsePathobiontsInnate immunityPaired samplesCXCL10Healthy 1-year-oldVirusA common polymorphism in the Intelectin-1 gene influences mucus plugging in severe asthma
Everman J, Sajuthi S, Liegeois M, Jackson N, Collet E, Peters M, Chioccioli M, Moore C, Patel B, Dyjack N, Powell R, Rios C, Montgomery M, Eng C, Elhawary J, Mak A, Hu D, Huntsman S, Salazar S, Feriani L, Fairbanks-Mahnke A, Zinnen G, Michel C, Gomez J, Zhang X, Medina V, Chu H, Cicuta P, Gordon E, Zeitlin P, Ortega V, Reisdorph N, Dunican E, Tang M, Elicker B, Henry T, Bleecker E, Castro M, Erzurum S, Israel E, Levy B, Mauger D, Meyers D, Sumino K, Gierada D, Hastie A, Moore W, Denlinger L, Jarjour N, Schiebler M, Wenzel S, Woodruff P, Rodriguez-Santana J, Pearson C, Burchard E, Fahy J, Seibold M. A common polymorphism in the Intelectin-1 gene influences mucus plugging in severe asthma. Nature Communications 2024, 15: 3900. PMID: 38724552, PMCID: PMC11082194, DOI: 10.1038/s41467-024-48034-5.Peer-Reviewed Original ResearchConceptsAirway epithelial cellsIntelectin-1Mucus pluggingGene expressionAirways of severe asthmaticsEpithelial cellsHuman airway epithelial cellsAirway epithelial brushingsMucus secretory cellsT2-high asthmaFormation of mucus plugsAssociated with protectionC-terminusGenetic variantsAirway mucus pluggingMolecular roleSecretory cellsSecreted componentsEpithelial brushingsT2-lowIL-13Mucus obstructionTarget pathwaysSevere asthmaticsClinical significanceIntegrated longitudinal multiomics study identifies immune programs associated with acute COVID-19 severity and mortality
Gygi J, Maguire C, Patel R, Shinde P, Konstorum A, Shannon C, Xu L, Hoch A, Jayavelu N, Haddad E, Network I, Reed E, Kraft M, McComsey G, Metcalf J, Ozonoff A, Esserman D, Cairns C, Rouphael N, Bosinger S, Kim-Schulze S, Krammer F, Rosen L, van Bakel H, Wilson M, Eckalbar W, Maecker H, Langelier C, Steen H, Altman M, Montgomery R, Levy O, Melamed E, Pulendran B, Diray-Arce J, Smolen K, Fragiadakis G, Becker P, Sekaly R, Ehrlich L, Fourati S, Peters B, Kleinstein S, Guan L. Integrated longitudinal multiomics study identifies immune programs associated with acute COVID-19 severity and mortality. Journal Of Clinical Investigation 2024, 134: e176640. PMID: 38690733, PMCID: PMC11060740, DOI: 10.1172/jci176640.Peer-Reviewed Original ResearchConceptsClinical outcomesImmune cascadeElevated levels of inflammatory cytokinesDisease severityLevels of inflammatory cytokinesFormation of neutrophil extracellular trapsAcute COVID-19 severityCritically ill patientsNeutrophil extracellular trapsDevelopment of therapiesCOVID-19 cohortCOVID-19 severityViral clearanceImmunosuppressive metabolitesDeep immunophenotypingMultiomic modelIFN-stimulated genesImmunophenotypic assessmentB cellsDisease courseEarly upregulationInflammatory cytokinesDisease progressionIFN inhibitorsExtracellular trapsHuman regulatory memory B cells defined by expression of TIM-1 and TIGIT are dysfunctional in multiple sclerosis
Varghese J, Kaskow B, von Glehn F, Case J, Li Z, Julé A, Berdan E, Sui S, Hu Y, Krishnan R, Chitnis T, Kuchroo V, Weiner H, Baecher-Allan C. Human regulatory memory B cells defined by expression of TIM-1 and TIGIT are dysfunctional in multiple sclerosis. Frontiers In Immunology 2024, 15: 1360219. PMID: 38745667, PMCID: PMC11091236, DOI: 10.3389/fimmu.2024.1360219.Peer-Reviewed Original ResearchConceptsMemory B cell subsetsMemory B cellsB cell subsetsT cell activationB cellsT cellsMultiple sclerosisIL-17ATIM-1Levels of CD4+ T cell activationAllogeneic CD4+ T cellsRelapsing-remittingAssociated with response to therapyAnti-CD20 treated patientsCD4+ T cell activationDouble positive (DPCD4+ T cellsExpression of TIM-1Genes associated with T-cell activationInduction of inflammatory markersInduce T cell proliferationHuman memory B cellsLack of cell surface markersRegulatory B cellsExpression of genes associated with T-cell activation
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