Adjunct Faculty
Adjunct faculty typically have an academic or research appointment at another institution and contribute or collaborate with one or more School of Medicine faculty members or programs.
Adjunct rank detailsVijay Kuchroo
Research
Publications
2026
IDH1-R132H enhances oncolytic HSV-1 therapy by facilitating viral entry and immune activation in glioma
Panagioti E, Kelley H, Ling A, Sejour L, Saini S, Goins W, Roberts D, Sotiriou S, Bryan Iorgulescu J, Dixon K, Yaffe M, Vlachos I, Castro M, Lawler S, Freeman G, Kuchroo V, Antonio Chiocca E, Cook C. IDH1-R132H enhances oncolytic HSV-1 therapy by facilitating viral entry and immune activation in glioma. Nature Communications 2026 PMID: 42310302, DOI: 10.1038/s41467-026-73974-5.Peer-Reviewed Original ResearchIDH1-R132Htherapeutic efficacyintratumoral administrationimmune activationoncolytic herpes simplex virus-1expression of poliovirus receptorpoliovirus receptorantitumor immune activityHSV-1 therapyelevated expressionT cell immunoreceptortumor-infiltrating leukocytesIDH1 R132H mutationmurine glioma modelsusceptibility to viral infectionsHSV-1 entry receptortumor cell apoptosisherpes simplex virus 1precision cancer treatmentoHSV-1TIGIT blockadeoncolytic virotherapypredictive biomarkersglioma modelimmune infiltrationInterleukin 23 promotes a pro-inflammatory Th17 cell state by stabilizing RORγt and suppressing glucocorticoid receptor activity
Yang D, Huang L, Yang J, Etxezarreta-Arrastoa O, Schramm M, Khodaverdian A, Acharya N, Krovi S, Dixon K, Cheng H, Wei K, Xia J, Cheng F, Nelson A, Abell K, Ren J, Yang V, Sikorski T, Annan R, Van Horn S, Traini C, Carlson T, Krishnan R, Stokes M, Sobel R, Yosef N, Anderson A, Kuchroo V. Interleukin 23 promotes a pro-inflammatory Th17 cell state by stabilizing RORγt and suppressing glucocorticoid receptor activity. Immunity 2026 PMID: 42285104, DOI: 10.1016/j.immuni.2026.05.016.Peer-Reviewed Original Researchchromodomain helicase DNA-binding protein 1transcription factorsautoimmune tissue inflammationIL-23Rcell statesDNA-binding protein 1glucocorticoid receptorIL-23tissue inflammationIL-17-producing T helper cellsepigenetic regulationinterleukin-23 receptorT helper cellsIL-12 receptorIL-23R signalingglucocorticoid receptor activationgene programnuclear translocationprotein 1interleukin-23IL-12RIL-12receptor activationtherapeutic targetreceptorsAn adaptive cellular source of IL-17A and IL-17F is critical for the induction of experimental autoimmune encephalomyelitis
Ho A, Huang L, Sandhu S, Xiao S, Sgodzai M, Ullerich E, Krishnan R, Schnell A, Kuchroo V. An adaptive cellular source of IL-17A and IL-17F is critical for the induction of experimental autoimmune encephalomyelitis. Science Immunology 2026, 11: eaee1481. PMID: 42030372, DOI: 10.1126/sciimmunol.aee1481.Peer-Reviewed Original ResearchConceptsexperimental autoimmune encephalomyelitisinduction of experimental autoimmune encephalomyelitisadoptive transfer modelIL-17EAE diseaseautoimmune encephalomyelitisIL-17AIL-17Fadoptive transfer model of experimental autoimmune encephalomyelitiscellular source of IL-17Amodel of experimental autoimmune encephalomyelitissource of IL-17Acellular source of IL-17source of IL-17T helper 17IL-17 signalingtranscriptional profilesIL-23T cellsautoimmune disordersB cellsinterleukin-17IL-17A/Fcellular sourceanimal modelsThe dual role of TOX in regulating TH1 and CD8+ T cell fate
Kye Y, Kuchroo V. The dual role of TOX in regulating TH1 and CD8+ T cell fate. Nature Immunology 2026, 27: 886-887. PMID: 41974962, DOI: 10.1038/s41590-026-02494-7.Peer-Reviewed Original ResearchInhibitory receptor agonists: Emerging strategies in immune modulation
Adam K, Suhail A, Kuchroo V, Vignali D. Inhibitory receptor agonists: Emerging strategies in immune modulation. Journal Of Experimental Medicine 2026, 223: e20241217. PMID: 41915422, DOI: 10.1084/jem.20241217.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsinhibitory receptorsantitumor T-cell responsesblockade of inhibitory receptorseffector T cell functionmanagement of autoimmunityT cell responsesexcessive immune activationT cell functionregulation of immune homeostasisCTLA-4PD-1cancer immunotherapyTim-3immune tolerancemechanism of actionpreclinical modelsagonistic antibodiesimmune activationimmunosuppressive potentialimmune homeostasisimmune modulationtherapeutic efficacyinflammatory disordersinflammatory diseasesclinical practiceAuthor Correction: Circadian circuits control plasticity of group 3 innate lymphoid cells by sustaining epigenetic configuration of RORγt
Bhattarai B, Antonova A, Fachi J, Hopkins L, McCullen M, Saini A, Oliveira S, Beatty W, Musiek E, Kuchroo V, Lazar M, Oltz E, Colonna M. Author Correction: Circadian circuits control plasticity of group 3 innate lymphoid cells by sustaining epigenetic configuration of RORγt. Nature Immunology 2026, 27: 1306-1306. PMID: 41896466, DOI: 10.1038/s41590-026-02507-5.Peer-Reviewed Original ResearchCD5L:p40, a novel heterodimeric regulator of type 2 inflammation
Wang C, Zaghouani S, Wallrapp A, Newcomer K, Greenfield E, Johnson J, Barilla R, Pawlak M, Christian E, Burkett P, Leabo M, Li P, Soto H, Chen R, Monell C, Brown M, Almo S, Singer M, Regev A, Kuchroo V. CD5L:p40, a novel heterodimeric regulator of type 2 inflammation. The Journal Of Immunology 2026, 215: vkaf348. PMID: 41847855, PMCID: PMC13017054, DOI: 10.1093/jimmun/vkaf348.Peer-Reviewed Original ResearchConceptsIL-23IL-12airway inflammationIL-12p40experimental model of colitiseffector Th17 cellsfunction of IL-12type 2 inflammationIL-13 expressionexperimental modelmodel of colitiscentral nervous systemTh17 cellsTh17 responsesTh2 responsesT cellsautoimmune inflammationmyeloid cellsTh1 differentiationIL-13inflammatory diseasesinflammatory conditionsmonoclonal antibodiesIL-12p35nervous system
2025
Immune dysfunction in Alzheimer disease
Butovsky O, Rosenzweig N, Kleemann K, Jorfi M, Kuchroo V, Tanzi R, Weiner H. Immune dysfunction in Alzheimer disease. Nature Reviews Neuroscience 2025, 27: 196-218. PMID: 41315874, PMCID: PMC13010386, DOI: 10.1038/s41583-025-00997-0.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsAlzheimer's diseasegenome-wide association studiesAD risk variantspathology of Alzheimer's diseaseamyloid plaque accumulationfeatures of ADimmune cellsassociation studiestau pathologyrisk variantsepigenetic reprogrammingperipheral immune alterationsimmune checkpoint inhibitionimmune cell crosstalkperipheral immune cellschronic peripheral inflammationadaptive immune pathwaysnext-generation therapiesimmune pathwaysgenetic riskhuman-derived datacheckpoint inhibitionimmune exhaustionimmune alterationsimmune dysfunctionCircadian circuits control plasticity of group 3 innate lymphoid cells by sustaining epigenetic configuration of RORγt
Bhattarai B, Antonova A, Fachi J, Hopkins L, McCullen M, Saini A, Oliveira S, Beatty W, Musiek E, Kuchroo V, Lazar M, Oltz E, Colonna M. Circadian circuits control plasticity of group 3 innate lymphoid cells by sustaining epigenetic configuration of RORγt. Nature Immunology 2025, 26: 1527-1539. PMID: 40804530, PMCID: PMC12633719, DOI: 10.1038/s41590-025-02240-5.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBasic-Leucine Zipper Transcription FactorsCell PlasticityCircadian RhythmCitrobacter rodentiumEnergy MetabolismEnterobacteriaceae InfectionsEpigenesis, GeneticImmunity, InnateInterferon-gammaInterleukin-22InterleukinsLymphocytesMiceMice, Inbred C57BLMice, KnockoutNuclear Receptor Subfamily 1, Group D, Member 1Nuclear Receptor Subfamily 1, Group F, Member 3Conceptsgroup 3 innate lymphoid cellsepigenetic configurationcis-regulatory elementsCitrobacter rodentium infectionsingle-cell multiomicsregulate clock genescircadian proteinsgut homeostasiscircadian circuitsmetabolic circuitsIL-22 productionclock genesIL-22Rev-erbARORC genemetabolic analysisgenesgut integritygene editingenergy metabolismgutnutrient absorptionlymphoid cellsinterleukin-22intestinal inflammationThe glycolytic reaction PGAM restrains Th17 pathogenicity and Th17-dependent autoimmunity
Wang C, Wagner A, Fessler J, DeTomaso D, Zaghouani S, Zhou Y, Pierce K, Sobel R, Clish C, Yosef N, Kuchroo V. The glycolytic reaction PGAM restrains Th17 pathogenicity and Th17-dependent autoimmunity. Cell Reports 2025, 44: 115799. PMID: 40482033, PMCID: PMC12443480, DOI: 10.1016/j.celrep.2025.115799.Peer-Reviewed Original ResearchConceptsnon-pathogenic phenotypespathogenic gene expression programsnegative regulatorpathogenic statesingle-cell RNA sequencinggene expression programspathogenic Th17 cell differentiationgene modulesphosphoglycerate mutaseRNA sequencingglycolytic enzymesexpression programsglycolytic reactionscell differentiationmetabolic shuntmetabolic stateTh17 cell differentiationpathogensadoptive transfer modelenzymeTh17 cellscellsglucose metabolismT helper 17effector differentiation