P. Kent Langston, PhD
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Dr. Kent Langston is an assistant professor of Pathology at Yale School of Medicine and a member of the Yale Center for Research on Aging (Y-Age). He received his Ph.D. from Harvard University for his work in Dr. Tiffany Horng's laboratory on metabolic regulation of macrophage activation and tolerance. He completed his postdoctoral training with Drs. Diane Mathis and Christophe Benoist in the Department of Immunology at Harvard Medical School. In the Mathis-Benoist laboratory, Dr. Langston elucidated the dynamics of physiological inflammatory responses to endurance exercise in skeletal muscles and discovered that appropriate regulation of such inflammation is required for the muscle-specific and organism-level metabolic adaptations and improved performance typical of training. Specifically, his work identified interferon-gamma as a T-cell and NK-cell effector molecule that is unleashed in Treg-deficient mice and is necessary and sufficient to impair muscle mitochondrial function to the detriment of endurance-exercise performance.
The Langston laboratory is further defining the cellular and molecular features of exercise-induced inflammatory responses in youth and during aging – an endeavor that is partly supported by an NIA/NIH K22 award – with an emphasis on elucidating how non-parenchymal cells sense exercise and regulate its benefits. An ultimate goal of this work is to design exercise-inspired interventions to combat modern afflictions associated with chronic inflammation, improve regeneration and performance after injury, reduce the pathology of musculoskeletal diseases, and combat age-related frailty (i.e., increase healthspan).
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Pathology
Assistant ProfessorPrimary
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Education & Training
- Postdoctoral Fellow
- Harvard Medical School (2025)
- PhD
- Harvard University, Immunometabolism (2019)
- BS (Hon)
- Wake Forest University, Chemistry (2014)
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ORCID
0000-0001-6655-1911
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Featured Publications
Regulatory T cells shield muscle mitochondria from interferon-γ–mediated damage to promote the beneficial effects of exercise
Langston P, Sun Y, Ryback B, Mueller A, Spiegelman B, Benoist C, Mathis D. Regulatory T cells shield muscle mitochondria from interferon-γ–mediated damage to promote the beneficial effects of exercise. Science Immunology 2023, 8: eadi5377. PMID: 37922340, PMCID: PMC10860652, DOI: 10.1126/sciimmunol.adi5377.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsHealth activitiesPerformance-enhancing effectsEffects of exercise trainingEffects of exerciseResponse to exerciseChronic exercise modelsExercise trainingPhysical performanceExercise modelType 2 diabetesExerciseCD4+ regulatory T cellsCardiovascular diseaseFoxp3+ CD4+ regulatory T cellsRegulatory T cellsSkeletal muscleT cellsInterferon-gMuscle mitochondriaEffector mechanismsMuscleInflammatory responseTherapeutic potentialDementiaMetabolic disruptionImmunological regulation of skeletal muscle adaptation to exercise
Langston P, Mathis D. Immunological regulation of skeletal muscle adaptation to exercise. Cell Metabolism 2024, 36: 1175-1183. PMID: 38670108, PMCID: PMC11153001, DOI: 10.1016/j.cmet.2024.04.001.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsCitationsAltmetricMeSH Keywords and ConceptsConceptsExercise immunologyBenefits of exerciseSkeletal muscle adaptationEffects of exerciseResponse to exerciseMaintenance of muscle homeostasisExercise adaptationMuscle adaptationExercise physiologyExercising muscleMusculoskeletal diseasesExerciseMuscle injuryMuscleSkeletal muscleHealth-promoting effectsMuscle biologyImmunological regulationExertionMuscle homeostasisExperimental muscle injuryConceptual frameworkImmunological basisSymptomsAge
2025
Regulatory T cells in brown adipose tissue safeguard thermogenesis by restraining interferon-γ–producing lymphocytes
Zammit N, Vargas-Castillo A, Langston P, Wang G, Zhou Y, Spiegelman B, Benoist C, Mathis D. Regulatory T cells in brown adipose tissue safeguard thermogenesis by restraining interferon-γ–producing lymphocytes. Science Immunology 2025, 10: eads0478. PMID: 40712046, PMCID: PMC12363373, DOI: 10.1126/sciimmunol.ads0478.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and Concepts
2023
Borrelia burgdorferi initiates early transcriptional re-programming in macrophages that supports long-term suppression of inflammation
Petnicki-Ocwieja T, McCarthy J, Powale U, Langston P, Helble J, Hu L. Borrelia burgdorferi initiates early transcriptional re-programming in macrophages that supports long-term suppression of inflammation. PLOS Pathogens 2023, 19: e1011886. PMID: 38157387, PMCID: PMC10783791, DOI: 10.1371/journal.ppat.1011886.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsLong-term infectionAconitate decarboxylase 1Regulation of immune pathwaysInnate immune memoryAttenuation of inflammationSuppression of inflammationLong-term suppression of inflammationMaintenance of suppressionLong-term suppressionHost immune responseAnalysis of macrophagesIn vivo infectionAnti-inflammatory modulatorIn vitro modelInflammatory manifestationsTranscriptional re-programmingInflammatory cellsCausative agent of Lyme diseaseComparative transcriptional analysisLyme carditisPhenotypic subsetsCellular re-programmingHypo-responsivenessImmune memoryInflammatory mediatorsA discrete ‘early-responder’ stromal-cell subtype orchestrates immunocyte recruitment to injured tissue
Yaghi O, Hanna B, Langston P, Michelson D, Jayewickreme T, Marin-Rodero M, Benoist C, Mathis D. A discrete ‘early-responder’ stromal-cell subtype orchestrates immunocyte recruitment to injured tissue. Nature Immunology 2023, 24: 2053-2067. PMID: 37932455, PMCID: PMC10792729, DOI: 10.1038/s41590-023-01669-w.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsMesenchymal stromal cellsStromal cellsMouse modelMouse model of muscular dystrophyModels of muscular dystrophyAcute injuryUnique surface markersRecruitment of neutrophilsResponse to injuryStromal cell subtypesImmunomodulatory programsImmunocyte recruitmentCell collaborationTissue regenerationStroma-specificTNF-aSurface markersDay 1IL-1BCell subtypesInflammatory programMuscular dystrophyInduce inflammationSubtypesOncostatin MSpatial enrichment of the type 1 interferon signature in the brain of a neuropsychiatric lupus murine model.
Aw E, Zhang Y, Yalcin E, Herrmann U, Lin SL, Langston K, Castrillon C, Ma M, Moffitt JR, Carroll MC. Spatial enrichment of the type 1 interferon signature in the brain of a neuropsychiatric lupus murine model. Brain Behav Immun 2023, 114: 511-522. PMID: 37369340, DOI: 10.1016/j.bbi.2023.06.021.Peer-Reviewed Original Research
2022
Tregs in visceral adipose tissue up-regulate circadian-clock expression to promote fitness and enforce a diurnal rhythm of lipolysis
Xiao T, Langston P, Muñoz-Rojas A, Jayewickreme T, Lazar M, Benoist C, Mathis D. Tregs in visceral adipose tissue up-regulate circadian-clock expression to promote fitness and enforce a diurnal rhythm of lipolysis. Science Immunology 2022, 7: eabl7641. PMID: 36179011, PMCID: PMC9769829, DOI: 10.1126/sciimmunol.abl7641.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsVisceral adipose tissueBmal1 deficiencyVisceral adipose tissue inflammationWeeks of high-fat diet feedingRegulatory T cellsAdipose tissueCircadian clock expressionTranscriptomic signaturesCore clock componentsLoss of fitnessHigh-fat diet feedingCore clock genesSuppression of lipolysisDiurnal rhythmNonlymphoid organsT cellsAdipose tissue lipolysisDiurnal regulationCircadian programTissue homeostasisAdipocyte lipolysisConstitutive activationDiet feedingUp-regulatedMetabolic stateThe potential for Treg-enhancing therapies in tissue, in particular skeletal muscle, regeneration
Hanna B, Yaghi O, Langston P, Mathis D. The potential for Treg-enhancing therapies in tissue, in particular skeletal muscle, regeneration. Clinical & Experimental Immunology 2022, 211: 138-148. PMID: 35972909, PMCID: PMC10019136, DOI: 10.1093/cei/uxac076.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsCitationsAltmetricMeSH Keywords and ConceptsConceptsT cellsFoxP3+CD4+ regulatory T cellsRegulatory T cellsSkeletal muscleTreg modulationGrowth factor dependenceTreg roleImmunological toleranceNonlymphoid tissuesTissue regenerationTregsChronic injuryGrowth factorTherapeutic modulationTissue repairTissue homeostasisTherapyTissueInjuryRepairMuscleFoxp3+CD4ImmunotherapyFibrosis
2021
Down-Regulation of a Profibrotic Transforming Growth Factor-β1/Cellular Communication Network Factor 2/Matrix Metalloprotease 9 Axis by Triamcinolone Improves Idiopathic Subglottic Stenosis
Treviño-Villarreal J, Reynolds J, Langston P, Thompson A, Mitchell J, Franco R. Down-Regulation of a Profibrotic Transforming Growth Factor-β1/Cellular Communication Network Factor 2/Matrix Metalloprotease 9 Axis by Triamcinolone Improves Idiopathic Subglottic Stenosis. American Journal Of Pathology 2021, 191: 1412-1430. PMID: 34111429, DOI: 10.1016/j.ajpath.2021.05.013.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsIdiopathic subglottic stenosisCellular communication network factor 2Matrix metalloprotease 9TGF-b1Subglottic stenosisPromoter regionHistone acetylationLife-threatening airwaySerial intralesional steroid injectionIntralesional steroid injectionBinding to promotersProgressive fibrotic diseaseSteroid injectionClinical outcomesProfibrotic markersProspective studyGlandular epitheliumStromal fibroblastsGlandular structuresMolecular markersFibrotic diseasesMetalloprotease 9Matrix of fibronectinMolecular underpinningsFibroblast infiltrationConditioned Media from Ultrasound‐treated C2C12 Myotubes Regulate Macrophage Inflammatory Responses
Yamaguchi A, Maeshige N, Langston P, Noguchi H, Ma X, Ichikawa Y, Uemura M, Kondo H, Fujino H. Conditioned Media from Ultrasound‐treated C2C12 Myotubes Regulate Macrophage Inflammatory Responses. The FASEB Journal 2021, 35 DOI: 10.1096/fasebj.2021.35.s1.00231.Peer-Reviewed Original ResearchConceptsConditioned mediumInflammatory responseAnti-inflammatory effectsC2C12 myotubesExtracellular vesiclesIL-1BLevels of IL-1bMRNA expressionExpression of IL-1bFacilitatory effectMRNA expression of pro-Bone marrow-derived macrophagesExpression levelsMurine bone marrow-derived macrophagesLevels of extracellular vesiclesAnti-inflammatory markersEV releaseMarrow-derived macrophagesExpression of pro-Ultrasound (USRelease of extracellular vesiclesAnti-inflammatory factorsExcessive tissue damageMacrophage inflammatory responseResponse of macrophages
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