2024
An autoimmune transcriptional circuit drives FOXP3+ regulatory T cell dysfunction
Sumida T, Lincoln M, He L, Park Y, Ota M, Oguchi A, Son R, Yi A, Stillwell H, Leissa G, Fujio K, Murakawa Y, Kulminski A, Epstein C, Bernstein B, Kellis M, Hafler D. An autoimmune transcriptional circuit drives FOXP3+ regulatory T cell dysfunction. Science Translational Medicine 2024, 16: eadp1720. PMID: 39196959, DOI: 10.1126/scitranslmed.adp1720.Peer-Reviewed Original ResearchConceptsForkhead box P3Autoimmune diseasesCD4<sup>+</sup>Foxp3<sup>+</sup> regulatory T cellsMultiple sclerosisFoxp3<sup>+</sup> regulatory T cellsRegulatory T cell dysfunctionPR domain zinc finger protein 1Zinc finger protein 1Glucocorticoid-regulated kinase 1Regulatory T cellsT cell dysfunctionDisorder of young adultsAutoimmune disease multiple sclerosisDisease multiple sclerosisExpression of serumTranscriptional circuitsEpigenomic profilingShort isoformPrevent autoimmunityUpstream regulatorT cellsHuman autoimmunityEvolutionary emergenceKinase 1Molecular mechanisms
2020
Epigenetic fine-mapping: identification of causal mechanisms for autoimmunity
Lincoln MR, Axisa PP, Hafler DA. Epigenetic fine-mapping: identification of causal mechanisms for autoimmunity. Current Opinion In Immunology 2020, 67: 50-56. PMID: 32977183, DOI: 10.1016/j.coi.2020.09.002.Peer-Reviewed Original ResearchConceptsGenome-wide association studiesMolecular mechanismsSusceptibility lociIndividual susceptibility lociFundamental genetic basisCausal molecular mechanismsPathogenic cell typesSpecific molecular mechanismsGenetic susceptibility lociEpigenetic techniquesGenetic basisGenetic lociAssociation studiesCell typesLociRecent advancesMechanismGeneticsAutoimmune diseasesSpectrum of autoimmunityCausal mechanismsEtiological mechanismsInflammatory diseasesTranslationAutoimmunity
2016
Solving Immunology?
Vodovotz Y, Xia A, Read EL, Bassaganya-Riera J, Hafler DA, Sontag E, Wang J, Tsang JS, Day JD, Kleinstein SH, Butte AJ, Altman MC, Hammond R, Sealfon SC. Solving Immunology? Trends In Immunology 2016, 38: 116-127. PMID: 27986392, PMCID: PMC5695553, DOI: 10.1016/j.it.2016.11.006.Peer-Reviewed Original Research
2004
4 Molecular Mimicry in Multiple Sclerosis Role of MHC-Altered Peptide Ligands (MAPL)
Lim D, Hafler D. 4 Molecular Mimicry in Multiple Sclerosis Role of MHC-Altered Peptide Ligands (MAPL). 2004, 45-55. PMCID: PMC7151874, DOI: 10.1016/b978-044451271-0.50004-1.Peer-Reviewed Original ResearchMicrobial peptidesMolecular mimicryMimicry hypothesisMolecular mechanismsMultiple sclerosisMolecular mimicry hypothesisDisease entityMajor pathogenic mechanismAttractive hypothesisMimicryPeptide ligandsMyelin proteinsSingle disease entityPathogenic mechanismsMultiple sclerosis lesionsCross-reacting antigenDirect evidenceDisease stageT cellsPeptidesSclerosis lesionsProteinDifferent disordersImmunological studiesMechanism