2025
Exogenous pyruvate is therapeutic against colitis by targeting cytosolic phospholipase A2
Hasan S, Ghani N, Zhao X, Good J, Liu C. Exogenous pyruvate is therapeutic against colitis by targeting cytosolic phospholipase A2. Genes & Diseases 2025, 12: 101571. DOI: 10.1016/j.gendis.2025.101571.Peer-Reviewed Original ResearchInflammatory bowel diseaseUlcerative colitisBowel diseaseDextran sodium sulfate-induced colitisChronic inflammatory bowel diseaseUlcerative colitis pathogenesisTight junction proteinsPhase of inflammationCytosolic phospholipase A2Immune dysregulationColitis pathogenesisReal-time PCRNFkB translocationCellular metabolitesColon histologyJunction proteinsInflammatory diseasesColitis modelQuantitative real-time PCRTherapeutic effectUlcerative colitis modelAction of pyruvateImmunofluorescence stainingColitisRNA sequencing analysisIncidence and predictors of immune checkpoint inhibitor treatment–related cognitive impairment in a racial and ethnic diverse population
Sayer M, Agrawal P, Ng D, Kagramanov D, Trudeau J, Othy S, Acharya M, Chan A. Incidence and predictors of immune checkpoint inhibitor treatment–related cognitive impairment in a racial and ethnic diverse population. Supportive Care In Cancer 2025, 33: 523. PMID: 40451933, PMCID: PMC12127230, DOI: 10.1007/s00520-025-09560-0.Peer-Reviewed Original ResearchConceptsIntroductionImmune checkpoint inhibitorsTherapy initiationPatient-reported outcomesGeneralized Estimating EquationsSignificant cognitive impairmentICI-treated patientsAnti-cancer immunityClinically significant cognitive impairmentCognitive functionCognitive impairmentTreatment-related cognitive impairmentPhysical functionCheckpoint inhibitorsMild to severe symptomsImpaired physical functionRisk patientsImmune dysregulationConcurrent symptomsInflammatory biomarkersPatient characteristicsSymptom scoresCancer therapyCognitive function scoresT-scoreTherapyIdentification 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 processSingle-cell elderly blood–CSF atlas implicates peripherally influenced immune dysregulation in normal pressure hydrocephalus
Duy P, Kiziltug E, Greenberg A, Mehta N, Hao L, Fortes C, Mullany S, Fan B, Manichaikul A, Teich A, Chan D, Alper S, Hyman B, Arnold S, McKhann G, Frosch M, Kahle K. Single-cell elderly blood–CSF atlas implicates peripherally influenced immune dysregulation in normal pressure hydrocephalus. Proceedings Of The National Academy Of Sciences Of The United States Of America 2025, 122: e2412159122. PMID: 40324076, PMCID: PMC12087963, DOI: 10.1073/pnas.2412159122.Peer-Reviewed Original ResearchConceptsIdiopathic normal pressure hydrocephalusNormal pressure hydrocephalusImmune dysregulationPeripheral bloodPressure hydrocephalusIdiopathic normal pressure hydrocephalus patientsProinflammatory alterationsVentricular CSFSingle-cell transcriptomicsINPH patientsCell populationsPatientsNeuroglial cellsCSFBloodHydrocephalusBaseline cognitive functionCognitive functionDysregulationMonocytesCharacterization and Clinical Implications of p53 Dysfunction in Patients With Myelodysplastic Syndromes
Zampini M, Riva E, Lanino L, Sauta E, Dos Reis R, Ejarque R, Maggioni G, Termanini A, Merlotti A, Campagna A, Dall’Olio L, Kulasekararaj A, Calvi M, Di Vito C, Bonometti A, Rahal D, Croci G, Boveri E, Gianelli U, Ponzoni M, Caselli R, Albertazzi S, Todisco G, Ubezio M, Crisafulli L, Frigo A, Lugli E, Mosca E, Acha P, Ghisletti S, Nicassio F, Santoro A, Diez-Campelo M, Solé F, Ades L, Platzbecker U, Santini V, Fenaux P, Haferlach T, Sallman D, Garcia-Manero G, Mavilio D, Remondini D, Castellani G, D'Amico S, Zeidan A, Komrokji R, Kordasti S, Ficara F, Della Porta M, Consortium C, Russo A, Travaglino E, Delleani M, Asti G, Ventura D, Tentori C, Buizza A, Brindisi M, Pinocchio N, Pesce F. Characterization and Clinical Implications of p53 Dysfunction in Patients With Myelodysplastic Syndromes. Journal Of Clinical Oncology 2025, 43: 2069-2083. PMID: 40315418, PMCID: PMC12169866, DOI: 10.1200/jco-24-02394.Peer-Reviewed Original ResearchConceptsMyelodysplastic syndromeP53 dysfunctionPhenotype of immune cellsClassification of myeloid neoplasmsIdentified high-risk patientsImpaired antigen presentationOptimal timing of therapeutic interventionsAbnormal p53 proteinHigh-risk patientsSubsets of patientsBone marrow progenitorsTiming of therapeutic interventionDesign of clinical trialsRecognition of patientsTumor protein 53Variant allele frequencyNF-kB pathwayInnovative immunotherapyMyeloid neoplasmsDismal outcomeMarrow progenitorsImmune dysregulationBiallelic inactivationImmune cellsPoor prognosisModeling bone marrow microenvironment and hematopoietic dysregulation in Gaucher disease through VavCre mediated Gba deletion
Belinsky G, Ruan J, Fattahi N, Mehta S, Boddupalli C, Mistry P, Nair S. Modeling bone marrow microenvironment and hematopoietic dysregulation in Gaucher disease through VavCre mediated Gba deletion. Human Molecular Genetics 2025, 34: 952-966. PMID: 40197748, PMCID: PMC12085781, DOI: 10.1093/hmg/ddaf045.Peer-Reviewed Original ResearchGD miceImmune dysregulationGaucher diseaseExpansion of monocytesImmune cell deconvolutionKnockout modelsBone marrow microenvironmentGlucocerebrosidase activityC57BL/6 J backgroundDeficient glucocerebrosidase activityGaucher cell infiltrationInfluence disease severityGD biomarkersGD pathologyGD pathophysiologyLysosomal storage disorderImmune landscapeDendritic cellsHematopoietic stemMarrow microenvironmentAccumulation of glucosylceramideVav-CreBone marrowCell infiltrationHematopoietic cellsMicroglial regulation of white matter development and its disruption in autism spectrum disorder
Canada K, Evans T, Pelphrey K. Microglial regulation of white matter development and its disruption in autism spectrum disorder. Cerebral Cortex 2025, 35: bhaf109. PMID: 40302613, DOI: 10.1093/cercor/bhaf109.Peer-Reviewed Original ResearchConceptsAutism spectrum disorderMaternal immune activationWhite matter developmentSpectrum disorderPresentation of autism spectrum disorderService of perceptionCortical brain regionsBrain-resident immune cellsWhite matterResident immune cellsSocial cognitionCore symptomsWhite matter abnormalitiesBrain regionsBrain functionNeurodevelopmental disordersOL lineage cellsImmune dysregulationEfficient neuronal signalingImmune activationImmune cellsCytokine releaseMicroglial reactivityHuman brainLineage cellsImmune dysregulation in glycogen storage disease 1b extends beyond neutropenia
Gehlhaar A, Shouval D, Santiago E, Ling G, McCourt B, Werner L, Yerushalmi B, Konnikova L. Immune dysregulation in glycogen storage disease 1b extends beyond neutropenia. Human Immunology 2025, 86: 111268. PMID: 40037121, DOI: 10.1016/j.humimm.2025.111268.Peer-Reviewed Original ResearchGlycogen storage disease type 1bGlycogen storage disease type 1b patientsImpaired immune cell traffickingClassic treatment strategiesUpregulation of CXCR3Effector memory phenotypeT cell populationsNatural killer cellsSystems immunology approachNon-classical monocytesImmune cell traffickingGlycogen storage disease 1bImmune defectsMemory phenotypeMultiple T cell populationsImmune landscapeRecurrent infectionsKiller cellsImmune dysregulationImmune impairmentImmunophenotypic characterizationSLC37A4 geneControl subjectsTreatment strategiesNeutrophil numbersHost-microbe multiomic profiling identifies distinct COVID-19 immune dysregulation in solid organ transplant recipients
Pickering H, Schaenman J, Phan H, Maguire C, Tsitsiklis A, Rouphael N, Higuita N, Atkinson M, Brakenridge S, Fung M, Messer W, Salehi-rad R, Altman M, Becker P, Bosinger S, Eckalbar W, Hoch A, Doni Jayavelu N, Kim-Schulze S, Jenkins M, Kleinstein S, Krammer F, Maecker H, Ozonoff A, Diray-Arce J, Shaw A, Baden L, Levy O, Reed E, Langelier C. Host-microbe multiomic profiling identifies distinct COVID-19 immune dysregulation in solid organ transplant recipients. Nature Communications 2025, 16: 586. PMID: 39794319, PMCID: PMC11723965, DOI: 10.1038/s41467-025-55823-z.Peer-Reviewed Original ResearchConceptsSolid organ transplant recipientsOrgan transplant recipientsTransplant recipientsInduction of pro-inflammatory genesSenescent T cellsTransitional B cellsImpaired viral clearanceImmune response to infectionAnti-spike IgG levelsNon-transplanted controlsFeatures of COVID-19Innate Immune Signaling PathwaysResponse to infectionPro-inflammatory genesSerum chemokinesViral clearanceImmune dysregulationT cellsImmune signaling pathwaysB cellsImmune featuresSex-matchedIgG levelsSevere diseaseTransplantationMultiomics dissection of human RAG deficiency reveals distinctive patterns of immune dysregulation but a common inflammatory signature
Bosticardo M, Dobbs K, Delmonte O, Martins A, Pala F, Kawai T, Kenney H, Magro G, Rosen L, Yamazaki Y, Yu H, Calzoni E, Lee Y, Liu C, Stoddard J, Niemela J, Fink D, Castagnoli R, Ramba M, Cheng A, Riley D, Oikonomou V, Shaw E, Belaid B, Keles S, Al-Herz W, Cancrini C, Cifaldi C, Baris S, Sharapova S, Schuetz C, Gennery A, Freeman A, Somech R, Choo S, Giliani S, Güngör T, Drozdov D, Meyts I, Moshous D, Neven B, Abraham R, El-Marsafy A, Kanariou M, King A, Licciardi F, Cruz-Muñoz M, Palma P, Poli C, Adeli M, Algeri M, Alroqi F, Bastard P, Bergerson J, Booth C, Brett A, Burns S, Butte M, Padem N, de la Morena M, Dbaibo G, de Ravin S, Dimitrova D, Djidjik R, Dorna M, Dutmer C, Elfeky R, Facchetti F, Fuleihan R, Geha R, Gonzalez-Granado L, Haljasmägi L, Ale H, Hayward A, Hifanova A, Ip W, Kaplan B, Kapoor N, Karakoc-Aydiner E, Kärner J, Keller M, Dávila Saldaña B, Kiykim A, Kuijpers T, Kuznetsova E, Latysheva E, Leiding J, Locatelli F, Alva-Lozada G, McCusker C, Celmeli F, Morsheimer M, Ozen A, Parvaneh N, Pasic S, Plebani A, Preece K, Prockop S, Sakovich I, Starkova E, Torgerson T, Verbsky J, Walter J, Ward B, Wisner E, Draper D, Myint-Hpu K, Truong P, Lionakis M, Similuk M, Walkiewicz M, Klion A, Holland S, Oguz C, Bogunovic D, Kisand K, Su H, Tsang J, Kuhns D, Villa A, Rosenzweig S, Pittaluga S, Notarangelo L, Ghosh R, Siefert B, Tokita M, Yan J, Jodarski C, Kamen M, Gore R, Reynolds-Lallement N, Lewis K, Bannon S, Borges A, Gentile N. Multiomics dissection of human RAG deficiency reveals distinctive patterns of immune dysregulation but a common inflammatory signature. Science Immunology 2025, 10: eadq1697. PMID: 39792639, PMCID: PMC12087669, DOI: 10.1126/sciimmunol.adq1697.Peer-Reviewed Original ResearchConceptsRAG deficiencyRecombination-activating geneImmune dysregulationInflammatory signaturePattern of immune dysregulationT helper 2B cell developmentType I interferonOmenn syndromeImmunological phenotypeImmune profileSelf-antigensB cellsClinical managementDefective TI interferonCellular indicesImmunopathologyPatientsMultiomics approachPhenotypeHypomorphic formDysregulationLineage-specific contributionsDeficiencyContribution of cellular immune dysregulation to myasthenia gravis pathology
Bayer A, Nowak R, O’Connor K. Contribution of cellular immune dysregulation to myasthenia gravis pathology. International Review Of Neurobiology 2025 DOI: 10.1016/bs.irn.2025.04.035.Peer-Reviewed Original ResearchMyasthenia gravisPersistence of autoimmunityB cell compartmentAbnormal immune responseDevelopment of TResponse to treatmentCellular compartmentsImpaired neuromuscular transmissionImmunopathology of MGTolerance checkpointsComplex immunopathologyImmune dysregulationPrevent autoimmunityT cellsAutoantibody productionPathological responseAutoimmune disordersB cellsDisease developmentAutoimmune diseasesDisease progressionImmune responseMultifactorial diseaseImmune systemNeuromuscular transmission
2024
Genetic and molecular drivers of scleroderma pathogenesis
Odell I. Genetic and molecular drivers of scleroderma pathogenesis. Clinics In Dermatology 2024, 43: 153-159. PMID: 39675445, PMCID: PMC12009687, DOI: 10.1016/j.clindermatol.2024.12.007.Peer-Reviewed Original ResearchGrowth factor signalingFactor signalingScleroderma pathogenesisActivated growth factor receptorsGenetic association studiesTherapeutic approachesMolecular driversHereditary hemorrhagic telangiectasiaAssociation studiesRegulatory genesGrowth factor receptorImmune regulatory genesGenetic studiesBiological insightsVascular endothelial cellsMolecular mechanismsHemorrhagic telangiectasiaImmune dysregulationClinical findingsVascular abnormalitiesHeterogeneous diseaseClinical phenotypeFactor receptorPatient phenotypesMultiple malignanciesCOVID-19-associated rhino-orbito-cerebral mucormycosis: a single center prospective study of 264 patients
Kim U, Perzia B, Kulkarni P, Rajiniganth M, Sundar B, Robin A, Shukla A, Maeng M. COVID-19-associated rhino-orbito-cerebral mucormycosis: a single center prospective study of 264 patients. Orbit 2024, 44: 24-33. PMID: 39051497, DOI: 10.1080/01676830.2024.2377249.Peer-Reviewed Original ResearchTranscutaneous retrobulbar amphotericin BRhino-orbital-cerebral mucormycosisRhino-orbitalCavernous sinusBiopsy-proven mucormycosisOutbreak of mucormycosisRetrobulbar amphotericin BNo light perceptionAssociated with high mortalityAssociated with increased mortalityEndoscopic sinus debridementPre-existing diabetesCerebral diseaseSymptomatic COVID-19Asymptomatic COVID-19Oral posaconazoleSinus debridementEye involvementWorse visionVision recoveryNew diabetesImmune dysregulationAmphotericin BClinical outcomesWeekly imagingMesenchymal stem cell-derived small extracellular vesicles alleviate the immunometabolic dysfunction in murine septic encephalopathy
Koutroulis I, Kratimenos P, Hoptay C, O’Brien W, Sanidas G, Byrd C, Triantafyllou M, Goldstein E, Jablonska B, Bharadwaj M, Gallo V, Freishtat R. Mesenchymal stem cell-derived small extracellular vesicles alleviate the immunometabolic dysfunction in murine septic encephalopathy. IScience 2024, 27: 110573. PMID: 39165840, PMCID: PMC11334791, DOI: 10.1016/j.isci.2024.110573.Peer-Reviewed Original ResearchCentral nervous systemSeptic encephalopathyStem cell (MSC)-derived small extracellular vesiclesSmall extracellular vesiclesDysregulated host response to infectionRestored aerobic metabolismLife-threatening organ dysfunctionLong-term sequelaeHost response to infectionExtracellular vesiclesMesenchymal stem cell-derived small extracellular vesiclesPro-inflammatory cytokinesCell-derived small extracellular vesiclesResponse to infectionStem cell-derived small extracellular vesiclesImmune dysregulationOrgan dysfunctionSusceptible to injurySeptic miceClinical symptomsClinical severityImmunometabolic dysfunctionIntravenous administrationDisease outcomeInfectious processA metabolic dependency of EBV can be targeted to hinder B cell transformation
Müller-Durovic B, Jäger J, Engelmann C, Schuhmachers P, Altermatt S, Schlup Y, Duthaler U, Makowiec C, Unterstab G, Roffeis S, Xhafa E, Assmann N, Trulsson F, Steiner R, Edwards-Hicks J, West J, Turner L, Develioglu L, Ivanek R, Azzi T, Dehio P, Berger C, Kuzmin D, Saboz S, Mautner J, Löliger J, Geigges M, Palianina D, Khanna N, Dirnhofer S, Münz C, Bantug G, Hess C, Berger C, Hess C, Koller M, Rossi S, Stampf S, Müller N. A metabolic dependency of EBV can be targeted to hinder B cell transformation. Science 2024, 385: eadk4898. PMID: 38781354, DOI: 10.1126/science.adk4898.Peer-Reviewed Original ResearchConceptsEpstein-Barr virusIndoleamine 2,3-dioxygenase 1B-cell transformationB cellsEBV-driven B-cell transformationIndoleamine 2,3-dioxygenase 1 expressionIndoleamine 2,3-dioxygenase 1 inhibitionInfection of B cellsEBV-infected B cellsEnzyme indoleamine 2,3-dioxygenase 1Epstein-Barr virus protein EBNA2Increased IDO1 activityNicotinamide adenine dinucleotideDevelopment of lymphomaEBV-related diseasesInfected B cellsHumanized miceTransplant patientsImmune dysregulationAdenosine triphosphateMitochondrial complex I activityComplex I activityMetabolic vulnerabilitiesIDO1 activitySerum signatureSingle-Cell Transcriptomic Analyses of Brain Parenchyma in Patients With New-Onset Refractory Status Epilepticus (NORSE)
Hanin A, Zhang L, Huttner A, Plu I, Mathon B, Bielle F, Navarro V, Hirsch L, Hafler D. Single-Cell Transcriptomic Analyses of Brain Parenchyma in Patients With New-Onset Refractory Status Epilepticus (NORSE). Neurology Neuroimmunology & Neuroinflammation 2024, 11: e200259. PMID: 38810181, PMCID: PMC11139018, DOI: 10.1212/nxi.0000000000200259.Peer-Reviewed Original ResearchConceptsNew-onset refractory status epilepticusTemporal lobe epilepsyGABAergic neuronsExcitatory neuronsInfiltrating MacrophagesProportion of GABAergic neuronsChronic temporal lobe epilepsyRefractory status epilepticusInhibitory GABAergic neuronsSingle-cell transcriptome analysisDecreased expression of genesDegree of demyelinationImmune disturbancesNeuronal excitabilityImmune dysregulationNew-onsetStatus epilepticusPoor outcomeRefractory epilepsyHealthy childrenMicroglial reactivitySingle-nucleus RNA sequencingNLRP3 inflammasome activationInflammatory responseLobe epilepsy#844 Renal manifestations of immune dysregulation, polyendocrinopathy, enteropathy, X-linked (IPEX) syndrome: an updated systematic review
Lee K, Hwang E, Shin J, Park J. #844 Renal manifestations of immune dysregulation, polyendocrinopathy, enteropathy, X-linked (IPEX) syndrome: an updated systematic review. Nephrology Dialysis Transplantation 2024, 39: gfae069-1209-844. DOI: 10.1093/ndt/gfae069.1209.Peer-Reviewed Original ResearchX-linked (IPEX) syndromeForkhead box protein 3Renal involvementIPEX syndromeIPEX patientsImmune dysregulationMembranous nephropathyCharacteristics of renal involvementManifestations of immune dysregulationDetecting renal involvementPatient outcomesCourse of glomerulonephritisGenotype-phenotype correlationResponse to treatmentMesangial proliferative glomerulonephritisRenal presentationRenal monitoringRenal manifestationsAutoimmune nephritisRenal biopsyNephrotic syndromeCase reportProliferative glomerulonephritisInterstitial nephritisPatientsThe foundation for investigating factor XI as a target for inhibition in human cardiovascular disease
Ali A, Becker R. The foundation for investigating factor XI as a target for inhibition in human cardiovascular disease. Journal Of Thrombosis And Thrombolysis 2024, 57: 1283-1296. PMID: 38662114, PMCID: PMC11645312, DOI: 10.1007/s11239-024-02985-0.Peer-Reviewed Original ResearchConceptsCardiovascular diseaseCoronary syndromeChronic coronary syndromeFactor XIManagement of patientsSusceptible to pharmacological inhibitionAcute coronary syndromeHuman cardiovascular diseaseAnticoagulant therapyImmune dysregulationSystemic inflammationAtrial fibrillationClinical trialsPharmacological inhibitionTargeted drugsThrombosisIschemic strokeReparative capabilitiesPhenotypic expressionEnvironmental triggersOxidative stressDay-to-day patient careMolecular eventsSyndromeDiseaseSecond‐line immunotherapy in new onset refractory status epilepticus
Hanin A, Muscal E, Hirsch L. Second‐line immunotherapy in new onset refractory status epilepticus. Epilepsia 2024, 65: 1203-1223. PMID: 38430119, DOI: 10.1111/epi.17933.Peer-Reviewed Original ResearchFebrile infection-related epilepsy syndromeSecond-line immunotherapyOnset refractory status epilepticusRefractory status epilepticusIntrathecal dexamethasoneStatus epilepticusCytokine levelsFunctional outcomesCerebrospinal fluid cytokine levelsInitiation of anakinraReduction of seizure frequencyLong-term functional outcomeResponse to treatmentSE onsetElevated serumFebrile infectionsImmune dysregulationLong-term disabilityTreatment initiationCase reportCytokine measurementsProspective studyAnakinraImmunotherapyTocilizumab
2023
Identification of unstable regulatory and autoreactive effector T cells that are expanded in patients with FOXP3 mutations
Borna Š, Lee E, Nideffer J, Ramachandran A, Wang B, Baker J, Mavers M, Lakshmanan U, Narula M, Garrett A, Schulze J, Olek S, Marois L, Gernez Y, Bhatia M, Chong H, Walter J, Kitcharoensakkul M, Lang A, Cooper M, Bertaina A, Roncarolo M, Meffre E, Bacchetta R. Identification of unstable regulatory and autoreactive effector T cells that are expanded in patients with FOXP3 mutations. Science Translational Medicine 2023, 15: eadg6822. PMID: 38117899, PMCID: PMC11070150, DOI: 10.1126/scitranslmed.adg6822.Peer-Reviewed Original ResearchConceptsAutoreactive effector T cellsEffector T cellsAutoreactive T cellsT cellsThymic-derived regulatory T cellsHematopoietic stem cell transplantationT cell receptor repertoireEctodermal dystrophy syndromeT-cell abnormalitiesRegulatory T cellsStem cell transplantationT cell autoreactivityCell receptor repertoireTranscription factor Foxp3FOXP3 mutationsImmunomodulatory treatmentImmune dysregulationPeripheral toleranceCell transplantationFoxp3 deficiencyTCR sequencingFactor Foxp3Patient's TCell abnormalitiesPatients
This site is protected by hCaptcha and its Privacy Policy and Terms of Service apply