Minh Pham
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About
Titles
PhD Candidate, Immunobiology
Biography
Minh received his BS in biochemistry and BA in chemical biology from Brandeis University in 2016, where he also finished his undergraduate thesis in the laboratory of Christopher Miller, PhD. In the following three years, Minh took interests in neuroimmunology and joined the laboratory of Howard Weiner, MD at the Ann Romney Center for Neurologic Diseases (ARCND) at Brigham and Women's Hospital and Harvard Medical School in Boston. There, he focused on a project determining the transcriptional gene signatures of various Th17 cell subsets implicated in autoimmune disorders such as multiple sclerosis and rheumatoid arthritis.
In 2019, Minh matriculated into Yale's Immunobiology PhD graduate program and subsequently joined the O'Connor Lab in May 2020. His investigative interests are in human translational immunology, particularly in B cells, antibodies, and their associated mechanisms of pathology in autoimmune myasthenia gravis (MG). His research integrates multiple clinical trials in order to answer questions that will inform clinicians, and help improve therapeutic strategies for patients with serious illnesses.
Outside of the lab, Minh enjoys cooking, fitness, hiking, and attending live music events. Minh is also a freelance wedding photographer and videographer.
Education & Training
- BS (Hon)
- Brandeis Univerisity, Biochemistry (2016)
Research
Research at a Glance
Yale Co-Authors
Frequent collaborators of Minh Pham's published research.
Publications Timeline
A big-picture view of Minh Pham's research output by year.
Gianvito Masi, MD
Kevin O'Connor, PhD
Richard Nowak, MD, MS
Frank Detterbeck, MD, FACS, FCCP
Robert Homer, MD, PhD
Steven Kleinstein, PhD
10Publications
254Citations
Publications
2023
Individual myasthenia gravis autoantibody clones can efficiently mediate multiple mechanisms of pathology
Pham M, Masi G, Patzina R, Obaid A, Oxendine S, Oh S, Payne A, Nowak R, O’Connor K. Individual myasthenia gravis autoantibody clones can efficiently mediate multiple mechanisms of pathology. Acta Neuropathologica 2023, 146: 319-336. PMID: 37344701, DOI: 10.1007/s00401-023-02603-y.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsMyasthenia gravisAntigenic modulationPathogenic mechanismsAutoimmune myasthenia gravisCurrent therapeutic approachesΑ-bungarotoxin bindingNicotinic acetylcholine receptorsReceptor blockadeSerum autoantibodiesAutoreactive clonesMonoclonal levelTherapeutic approachesMonoclonal autoantibodiesAcetylcholine receptorsComplement activationAutoantibodiesAChR subunitsJurkat cell lineDistinct molecular mechanismsPathogenic profilePathogenic capacityPathologyCell-based assaysMAbsPatientsClinicoserological insights into patients with immune checkpoint inhibitor‐induced myasthenia gravis
Masi G, Pham M, Karatz T, Oh S, Payne A, Nowak R, Howard J, Guptill J, Juel V, O'Connor K. Clinicoserological insights into patients with immune checkpoint inhibitor‐induced myasthenia gravis. Annals Of Clinical And Translational Neurology 2023, 10: 825-831. PMID: 36924454, PMCID: PMC10187728, DOI: 10.1002/acn3.51761.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and Concepts
2022
The clinical need for clustered AChR cell-based assay testing of seronegative MG
Masi G, Li Y, Karatz T, Pham MC, Oxendine SR, Nowak RJ, Guptill JT, O'Connor KC. The clinical need for clustered AChR cell-based assay testing of seronegative MG. Journal Of Neuroimmunology 2022, 367: 577850. PMID: 35366559, PMCID: PMC9106915, DOI: 10.1016/j.jneuroim.2022.577850.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsSNMG patientsMyasthenia gravisAChR-specific B cellsClinical needAcetylcholine receptor autoantibodiesSeronegative MG patientsSeronegative myasthenia gravisCell-based assaysAutoantibody positivityTrial eligibilityMG patientsReceptor autoantibodiesPatientsB cellsU.S. CentersNew treatmentsAssaysGravisAutoantibodiesSerostatusAChRPositivity
2021
Elevated N-Linked Glycosylation of IgG V Regions in Myasthenia Gravis Disease Subtypes.
Mandel-Brehm C, Fichtner ML, Jiang R, Winton VJ, Vazquez SE, Pham MC, Hoehn KB, Kelleher NL, Nowak RJ, Kleinstein SH, Wilson MR, DeRisi JL, O'Connor KC. Elevated N-Linked Glycosylation of IgG V Regions in Myasthenia Gravis Disease Subtypes. The Journal Of Immunology 2021, 207: 2005-2014. PMID: 34544801, PMCID: PMC8492536, DOI: 10.4049/jimmunol.2100225.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsMyasthenia gravisB-cell-mediated autoimmune diseasesBCR repertoireCell-mediated autoimmune diseaseTotal BCR repertoireTotal circulating IgGSubset of patientsB cell repertoireElevated NGene segment usageMG subtypesAutoimmune disordersAutoimmune diseasesHealthy donorsCell repertoireDisease subtypesDistinct subtypesReceptor repertoireAdaptive immune receptor repertoiresV regionsAutoantigen bindingPatientsSegment usageSubtypesImmune receptor repertoires
2020
Aberrant expression of USF2 in refractory rheumatoid arthritis and its regulation of proinflammatory cytokines in Th17 cells
Hu D, Tjon E, Andersson K, Molica G, Pham M, Healy B, Murugaiyan G, Pochet N, Kuchroo V, Bokarewa M, Weiner H. Aberrant expression of USF2 in refractory rheumatoid arthritis and its regulation of proinflammatory cytokines in Th17 cells. Proceedings Of The National Academy Of Sciences Of The United States Of America 2020, 117: 30639-30648. PMID: 33203678, PMCID: PMC7720234, DOI: 10.1073/pnas.2007935117.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAntirheumatic AgentsArthritis, RheumatoidBiomarkersCD4 AntigensCD4-Positive T-LymphocytesCytokinesGene ExpressionGene Expression ProfilingHumansInflammation MediatorsReceptors, CCR6Receptors, CXCR3RNA, Small InterferingSignal TransductionTh17 CellsTumor Necrosis Factor-alphaUpstream Stimulatory FactorsConceptsAnti-TNF therapyRefractory rheumatoid arthritisRheumatoid arthritisTh17 cellsT cellsProinflammatory cytokinesHigh-throughput gene expression analysisIL-17-producing Th17 cellsSignature genesDistinct gene expression profilesTranscription factor T-betProinflammatory cytokine IL-17ATranscription factor USF2Cytokines IL-17APathogenic Th17 cellsGene expression profilesGene expression analysisGranulocyte-macrophage colony-stimulating factorPotential therapeutic approachShort hairpin RNAColony-stimulating factorRA patientsIL-17ATh17 responsesExpression analysisThymus-derived B cell clones persist in the circulation after thymectomy in myasthenia gravis
Jiang R, Hoehn KB, Lee CS, Pham MC, Homer RJ, Detterbeck FC, Aban I, Jacobson L, Vincent A, Nowak RJ, Kaminski HJ, Kleinstein SH, O'Connor KC. Thymus-derived B cell clones persist in the circulation after thymectomy in myasthenia gravis. Proceedings Of The National Academy Of Sciences Of The United States Of America 2020, 117: 30649-30660. PMID: 33199596, PMCID: PMC7720237, DOI: 10.1073/pnas.2007206117.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAdolescentAdultAutoantibodiesBiomarkersB-LymphocytesClonal EvolutionClonal Selection, Antigen-MediatedDisease SusceptibilityFemaleHumansLymphocyte CountMaleMiddle AgedModels, BiologicalMyasthenia GravisRadioimmunoassayReceptors, CholinergicThymectomyThymus GlandV(D)J RecombinationYoung AdultConceptsB cell clonesMyasthenia gravisB cell repertoireB cellsCell clonesPlasma cellsCell repertoireAdditional immunosuppressive treatmentDiminished clinical responseThymic lymphofollicular hyperplasiaComplete stable remissionMajority of patientsAntigen-experienced B cellsRandomized clinical trialsClinical symptom measuresAChR autoantibodiesImmunosuppressive treatmentSteroid doseAutoantibody titersMG thymusClinical responseStable remissionClinical scoresAutoimmune diseasesClinical trialsTwo mAbs take a stab at influenza's NActive site.
Pham MC, O'Connor KC. Two mAbs take a stab at influenza's NActive site. Science Immunology 2020, 5 PMID: 33158977, DOI: 10.1126/sciimmunol.abf4907.Peer-Reviewed Original ResearchAltmetricSingle-cell repertoire tracing identifies rituximab-resistant B cells during myasthenia gravis relapses
Jiang R, Fichtner ML, Hoehn KB, Pham MC, Stathopoulos P, Nowak RJ, Kleinstein SH, O'Connor KC. Single-cell repertoire tracing identifies rituximab-resistant B cells during myasthenia gravis relapses. JCI Insight 2020, 5 PMID: 32573488, PMCID: PMC7453893, DOI: 10.1172/jci.insight.136471.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsMuscle-specific kinase myasthenia gravisMemory B cellsB cell subsetsAntibody-secreting cellsB cellsCell subsetsAutoantibody-producing B cellsB-cell depleting therapyCell-depleting therapyB cell clonesB cell survivalGene expression signaturesMyasthenia gravisAutoimmune disordersRelapseB cell samplesReceptor profilingCell clonesExpression signaturesRituximabTherapyCell survivalCellsTreatmentCell samples
2017
Transcriptional signature of human pro-inflammatory TH17 cells identifies reduced IL10 gene expression in multiple sclerosis
Hu D, Notarbartolo S, Croonenborghs T, Patel B, Cialic R, Yang TH, Aschenbrenner D, Andersson KM, Gattorno M, Pham M, Kivisakk P, Pierre IV, Lee Y, Kiani K, Bokarewa M, Tjon E, Pochet N, Sallusto F, Kuchroo VK, Weiner HL. Transcriptional signature of human pro-inflammatory TH17 cells identifies reduced IL10 gene expression in multiple sclerosis. Nature Communications 2017, 8: 1600. PMID: 29150604, PMCID: PMC5693957, DOI: 10.1038/s41467-017-01571-8.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsPathogenic Th17 cellsTh17 cellsExperimental autoimmune encephalomyelitisMultiple sclerosisTh1/17 cellsPro-inflammatory TH17 cellsExpression of CXCR3Human autoimmune diseasesIL10 gene expressionEffect of treatmentMolecular signaturesBlood IFNAutoimmune encephalomyelitisAutoimmune diseasesHealthy controlsDistinct transcriptional profilesT cellsGene signatureReduced expressionHigh expressionTranscriptional signatureSignature genesSclerosisIL10IFNMolecular determinants of permeation in a fluoride-specific ion channel.
Last NB, Sun S, Pham MC, Miller C. Molecular determinants of permeation in a fluoride-specific ion channel. Elife 2017, 6 PMID: 28952925, DOI: 10.7554/eLife.31259.Peer-Reviewed Original Research
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