2025
Medications for opioid use disorder shape immune responses during chronic HIV infection
Collora J, Steinhauser S, Davenport T, Lin D, Eshetu A, Zeidi S, Kim R, Frank C, Kluger Y, Springer S, Ho Y. Medications for opioid use disorder shape immune responses during chronic HIV infection. Cell Reports Medicine 2025, 6: 102159. PMID: 40460829, PMCID: PMC12208330, DOI: 10.1016/j.xcrm.2025.102159.Peer-Reviewed Original ResearchConceptsOpioid use disorderTumor necrosis factorImmune responseHIV infectionAssociated with HIV replicationCytotoxic T cell populationsRisk of opioid use disorderUse disorderPeripheral blood immune cellsI interferonChronic HIV infectionRNA expressionPartial agonist buprenorphineT cell populationsShape immune responsesBlood immune cellsType I interferonImprove immune responsesAgonist buprenorphineAgonist methadoneHIV expressionAntagonist naltrexoneHIV replicationImmune profileImmune cellsCutaneous lupus features specialized stromal niches and altered retroelement expression
Gehlhausen J, Kong Y, Baker E, Ramachandran S, Koumpouras F, Ko C, Vesely M, Little A, Damsky W, King B, Iwasaki A. Cutaneous lupus features specialized stromal niches and altered retroelement expression. Journal Of Investigative Dermatology 2025 PMID: 40409678, DOI: 10.1016/j.jid.2025.04.033.Peer-Reviewed Original ResearchRetroelement expressionCGAS-STING pathwayRIG-IType I interferonCutaneous lupusCGAS-STINGElevated expression of genesPathway enrichment analysisI interferonExpression of genesResponse to type I interferonsLupus skinRetroelement familiesInterferon-stimulated genesNucleic acid signalsApoptotic signalingSingle-cell RNAMultiple cell typesAcid signalingEnrichment analysisInflammatory cell recruitmentType II interferonInflammatory skin diseaseTumor necrosis factorCell typesThe cold immunological landscape of ATM-deficient cancers
Sinha S, Ng V, Novaj A, Zhu Y, Yazaki S, Pei X, Derakhshan F, Pareja F, Setton J, Naulin F, Beltrán-Visiedo M, Shin E, Longhini A, Gardner R, Ma J, Ma K, Roulston A, Morris S, Koehler M, Powell S, Rosen E, Galluzzi L, Reis-Filho J, Khan A, Riaz N. The cold immunological landscape of ATM-deficient cancers. Journal For ImmunoTherapy Of Cancer 2025, 13: e010548. PMID: 40350205, PMCID: PMC12067784, DOI: 10.1136/jitc-2024-010548.Peer-Reviewed Original ResearchConceptsImmune checkpoint blockadeCheckpoint blockadeTumor immunogenicityCell infiltrationLung cancerResponse to immune checkpoint blockadeNull tumorsATR inhibitionImmune effector cell infiltrationDesign of novel combination therapiesI interferonATM-deficient cancersEffector cell infiltrationEnhance tumor immunogenicityIncreasing tumor antigenicityNovel combination therapiesImmune cell infiltrationImmune cell recruitmentTriple-negative breastType I IFN signalingActivity of etoposideSynthetic lethal strategyActivation of type I interferonDefective DNA repairType I interferonYou know my NAMs
Ghosh S, Rothlin C. You know my NAMs. Immunity 2025, 58: 1179-1181. PMID: 40367920, DOI: 10.1016/j.immuni.2025.04.025.Peer-Reviewed Original ResearchType I interferons induce guanylate-binding proteins and lysosomal defense in hepatocytes to control malaria
Marques-da-Silva C, Schmidt-Silva C, Bowers C, Charles-Chess N, Samuel C, Shiau J, Park E, Yuan Z, Kim B, Kyle D, Harty J, MacMicking J, Kurup S. Type I interferons induce guanylate-binding proteins and lysosomal defense in hepatocytes to control malaria. Cell Host & Microbe 2025, 33: 529-544.e9. PMID: 40168996, DOI: 10.1016/j.chom.2025.03.008.Peer-Reviewed Original ResearchConceptsGuanylate-binding proteinsType I interferonPlasmodium infectionI interferonParasitophorous vacuoleLiver-stage malariaNon-immune cellsInfected host cellsCaspase-1 inflammasomeNADPH oxidase 2Clinical malariaControl malariaLysosomal fusionAntimicrobial programPlasmodium parasitesHost cellsInfected erythrocytesProtective immunityMalariaPlasmodiumGenetic inhibitionCaspase-1Immunization programsImmune circuitsMouse hepatocytesSelective STING Activation in Intratumoral Myeloid Cells via CCR2-Directed Antibody–Drug Conjugate TAK-500
Appleman V, Matsuda A, Ganno M, Zhang D, Rosentrater E, Lopez A, Porciuncula A, Hatten T, Christensen C, Merrigan S, Lee H, Lee M, Wang C, Dong L, Huang J, Iartchouk N, Wang J, Xu H, Yoneyama T, Piatkov K, Haridas S, Harbison C, Gregory R, Parent A, Lineberry N, Arendt C, Schalper K, Abu-Yousif A. Selective STING Activation in Intratumoral Myeloid Cells via CCR2-Directed Antibody–Drug Conjugate TAK-500. Cancer Immunology Research 2025, 13: 661-679. PMID: 39918395, PMCID: PMC12046323, DOI: 10.1158/2326-6066.cir-24-0103.Peer-Reviewed Original ResearchIntratumoral myeloid cellsMyeloid cellsTumor microenvironmentImmune responseCCR2+ cellsI interferonImmunosuppressive myeloid populationsImmune activation in vitroImmune cell markersLocal immune activationMurine tumor modelsAdaptive immune responsesAntibody drug conjugatesType I interferonAntitumor immunityInnate immune responseMyeloid populationsSTING agonistsSolid tumorsCCR2 proteinImmune activationTumor modelCell markersHuman tumorsAdaptive immunityInterferon-Stimulated Genes and Immune Metabolites as Broad-Spectrum Biomarkers for Viral Infections
Huang C, Laurent-Rolle M, Grove T, Hsu J. Interferon-Stimulated Genes and Immune Metabolites as Broad-Spectrum Biomarkers for Viral Infections. Viruses 2025, 17: 132. PMID: 39861921, PMCID: PMC11768885, DOI: 10.3390/v17010132.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsInterferon-stimulated genesReceiver Operating CharacteristicViral infectionAntiviral functionType I interferonTarget various stagesIFN-II interferonViral replicationClinical practiceDiagnostic potentialClinical applicationProtein levelsBiomarkersImmune defenseInfectionViral pathogensMetabolitesBroad spectrumGenesEffective translationMultiomics 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 contributionsDeficiency
2024
The amalgam of naive CD4+ T cell transcriptional states is reconfigured by helminth infection to dampen the amplitude of the immune response
Even Z, Meli A, Tyagi A, Vidyarthi A, Briggs N, de Kouchkovsky D, Kong Y, Wang Y, Waizman D, Rice T, De Kumar B, Wang X, Palm N, Craft J, Basu M, Ghosh S, Rothlin C. The amalgam of naive CD4+ T cell transcriptional states is reconfigured by helminth infection to dampen the amplitude of the immune response. Immunity 2024, 57: 1893-1907.e6. PMID: 39096910, PMCID: PMC11421571, DOI: 10.1016/j.immuni.2024.07.006.Peer-Reviewed Original ResearchT cell receptorImmune responseNaive CD4<sup>+</sup> T cellsCD4<sup>+</sup> T cellsIFN-IHelminth infectionsNippostrongylus brasiliensis infectionDecreased immune responseType I interferonNaive TT cellsMemory-likeUnrelated antigensTranscriptional changesExtracellular matrixSPF miceCell receptorsI interferonGerm-freeResponse to certain environmental cuesInfectionMiceFunctional changesCell transcriptional statesTranscriptional heterogeneityIron Chelation Therapy Elicits Innate Immune Control of Metastatic Ovarian Cancer.
Sandoval T, Salvagno C, Chae C, Awasthi D, Giovanelli P, Marin Falco M, Hwang S, Teran-Cabanillas E, Suominen L, Yamazaki T, Kuo H, Moyer J, Martin M, Manohar J, Kim K, Sierra M, Ramos Y, Tan C, Emmanuelli A, Song M, Morales D, Zamarin D, Frey M, Cantillo E, Chapman-Davis E, Holcomb K, Mason C, Galluzzi L, Ni Zhou Z, Vaharautio A, Cloonan S, Cubillos-Ruiz J. Iron Chelation Therapy Elicits Innate Immune Control of Metastatic Ovarian Cancer. Cancer Discovery 2024, 14: 1901-1921. PMID: 39073085, PMCID: PMC11452292, DOI: 10.1158/2159-8290.cd-23-1451.Peer-Reviewed Original ResearchNatural killerOvarian cancerFDA-approved iron chelatorIron chelatorsAlternative immunotherapeutic strategyI interferonActivated natural killerSurvival of miceOvarian cancer cellsType I IFN responseProduction of type I interferonsHallmarks of cancerType I interferonImmunostimulatory stateInnate immune responseMetastatic diseaseImmunotherapeutic strategiesOverexpression of moleculesTumor microenvironmentDisease progressionImmunomodulatory effectsImmune responseCancer cellsConcomitant activationDNA damage responseSerine Depletion Promotes Antitumor Immunity by Activating Mitochondrial DNA-Mediated cGAS-STING Signaling.
Saha S, Ghosh M, Li J, Wen A, Galluzzi L, Martinez L, Montrose D. Serine Depletion Promotes Antitumor Immunity by Activating Mitochondrial DNA-Mediated cGAS-STING Signaling. Cancer Research 2024, 84: 2645-2659. PMID: 38861367, PMCID: PMC11326969, DOI: 10.1158/0008-5472.can-23-1788.Peer-Reviewed Original ResearchAnti-tumor immunityImmune checkpoint inhibitors targeting PD-1Improved response to immune checkpoint inhibitorsCheckpoint inhibitors targeting PD-1Infiltration of immune effector cellsSuppressors of anti-tumor immunityColorectal cancerResponse to immune checkpoint inhibitorsEnhance tumor immunogenicityI interferonImmune checkpoint inhibitorsT-cell depletionCancer metabolismSerine deprivationImmune effector cellsSensitivity of tumorsType I IFN signalingAnti-neoplastic effectsImmune-enhancing effectsDisrupted metabolic pathwaysColorectal cancer cellsType I interferonCheckpoint inhibitorsIntratumoral infiltrationPD-1Macrophages restrain pathological interferon responses during viral respiratory infection
Rodriguez-Morales P, Hoagland D, Mann A, Yu S, Lai A, Baez Vazquez A, Medzhitov R, Franklin R. Macrophages restrain pathological interferon responses during viral respiratory infection. The Journal Of Immunology 2024, 212: 0536_5144-0536_5144. DOI: 10.4049/jimmunol.212.supp.0536.5144.Peer-Reviewed Original ResearchIFN-I productionOncostatin MBlockade of IFN-I signalingViral stimuliEpithelial cellsIFN-IOSM-deficient miceViral respiratory infectionsTriggered by infectionInflammation-induced pathologyLung epithelial cellsIFN-I responseIFN-I signalingRegulation of inflammationType I interferonPoly(I:CAcute blockadeCytokine oncostatin MRespiratory infectionsUncontrolled inflammationInflammatory responseI interferonInterferon responseRespiratory tractMiceRegional European genetic ancestry predicts type I interferon level and risk of severe viral infection
Nln I, Shum J, Ghodke-Puranik Y, Tipon R, Triese D, Amin S, Makol A, Osborn T, Chowdhary V, Thanarajasingam U, Muskardin T, Oke V, Gunnarsson I, Zickert A, Zervou M, Boumpas D, Svenungsson E, Goulielmos G, Niewold T. Regional European genetic ancestry predicts type I interferon level and risk of severe viral infection. QJM 2024, 117: 581-588. PMID: 38530799, PMCID: PMC11389909, DOI: 10.1093/qjmed/hcae052.Peer-Reviewed Original ResearchType I IFN levelsViral infection outcomesI interferonLupus patientsEuropean genetic ancestryInfection outcomesAnti-viral cytokinesSevere viral infectionsType I interferon levelsHost genetic factorsRisk of severe viral infectionsSevere organ failureI interferon levelsType I IFNType I interferonVirus prior to infectionViral hepatitisOrgan failureGenetic testingViral infectionI IFNOutcome dataHost defenseGenetic factorsGenetic ancestryA cluster of type I interferon-regulated genes associates with disease activity and prognosis in patients with IgA nephropathy
Qu S, Gan T, Wang Y, Qi Y, Zhang Y, Berthier C, Liu L, Shi S, Lv J, Zhang H, Zhou X. A cluster of type I interferon-regulated genes associates with disease activity and prognosis in patients with IgA nephropathy. International Immunopharmacology 2024, 131: 111920. PMID: 38522142, DOI: 10.1016/j.intimp.2024.111920.Peer-Reviewed Original ResearchIFN-regulated genesIFN-scoreIgAN patientsIgA nephropathyIFN-ITubular atrophy/interstitial fibrosisHigher IFN levelsCox regression analysisPathogenesis of IgA nephropathyType I interferonCross-sectional studyGross hematuriaMucosal infectionsRenal outcomesDisease activityIFN scoreInduce high levelsIFN levelsHealthy controlsMesangial hypercellularityIgANI interferonPatientsTherapeutic targetMicrobial infectionsAdaptive inhibition of CGAS signaling by TREX1
Lira M, Vanpouille-Box C, Galluzzi L. Adaptive inhibition of CGAS signaling by TREX1. Trends In Cancer 2024, 10: 177-179. PMID: 38355355, PMCID: PMC11075008, DOI: 10.1016/j.trecan.2024.02.001.Peer-Reviewed Original ResearchPotential role of RhoA GTPase regulation in type interferon signaling in systemic lupus erythematosus
Fan W, Wei B, Chen X, Zhang Y, Xiao P, Li K, Zhang Y, Huang J, Leng L, Bucala R. Potential role of RhoA GTPase regulation in type interferon signaling in systemic lupus erythematosus. Arthritis Research & Therapy 2024, 26: 31. PMID: 38243295, PMCID: PMC10799493, DOI: 10.1186/s13075-024-03263-3.Peer-Reviewed Original ResearchConceptsPeripheral blood mononuclear cellsRhoA GTPaseExpression levelsTreatment of SLEFunctions of RhoA.Knockdown of RhoAI IFN-stimulated genesSiRNA-mediated knockdownI interferonEnzyme-linked immunoassayIFN-stimulated genesGTPase signalingExpression levels of RhoASLE patientsLevels of RhoALupus erythematosusSLE peripheral blood mononuclear cellsGTPase regulatorHealthy controlsExpression of RhoAResponse pathwaysReporter gene assayRhoAType I IFN signalingSignal transducer
2023
COVID‐19 mRNA vaccine, but not a viral vector‐based vaccine, promotes neutralizing anti‐type I interferon autoantibody production in a small group of healthy individuals
Xu W, Wen X, Cong X, Jiang W. COVID‐19 mRNA vaccine, but not a viral vector‐based vaccine, promotes neutralizing anti‐type I interferon autoantibody production in a small group of healthy individuals. Journal Of Medical Virology 2023, 95: e29137. PMID: 37792386, PMCID: PMC10603818, DOI: 10.1002/jmv.29137.Peer-Reviewed Original ResearchConceptsViral vector-based vaccinesCOVID-19 mRNA vaccinesVector-based vaccinesGroup of healthy individualsMRNA vaccinesHealthy individualsPlasma levelsAnti-type I IFN autoantibodiesI interferonLevels of IgG autoantibodiesEvaluate plasma levelsHuman self-antigensPost-COVID-19 vaccinationCOVID-19 vaccineImpaired immune defenseInduce adverse eventsBaseline in vitroIncreased antibody levelsSARS-CoV-2 infectionSARS-CoV-2 antigensType I IFNType I interferonAutoantibody productionSelf-antigensInduce autoimmunitySREBP2 regulates the endothelial response to cytokines via direct transcriptional activation of KLF6
Fowler J, Boutagy N, Zhang R, Horikami D, Whalen M, Romanoski C, Sessa W. SREBP2 regulates the endothelial response to cytokines via direct transcriptional activation of KLF6. Journal Of Lipid Research 2023, 64: 100411. PMID: 37437844, PMCID: PMC10407908, DOI: 10.1016/j.jlr.2023.100411.Peer-Reviewed Original ResearchConceptsDirect transcriptional activationTranscriptional activationEndothelial cellsChemokine expressionChromatin immunoprecipitation sequencingCholesterol homeostasisSterol-responsive genesPro-inflammatory chemokinesLipid-lowering drugsAdaptive immune responsesPro-inflammatory genesTranscription factor SREBP2Endogenous cholesterol synthesisImmunoprecipitation sequencingResponsive genesMechanism of actionPromoter regionCardiovascular riskAtherosclerotic diseaseInflammatory phenotypeImmune modulationCardiovascular diseaseImmune responseInflammatory stimuliI interferonInflammatory and interferon gene expression signatures in patients with mitochondrial disease
Warren E, Gordon-Lipkin E, Cheung F, Chen J, Mukherjee A, Apps R, Tsang J, Jetmore J, Schlein M, Kruk S, Lei Y, West A, McGuire P. Inflammatory and interferon gene expression signatures in patients with mitochondrial disease. Journal Of Translational Medicine 2023, 21: 331. PMID: 37208779, PMCID: PMC10199642, DOI: 10.1186/s12967-023-04180-w.Peer-Reviewed Original ResearchConceptsMTD patientsHealthy controlsMitochondrial dysfunctionAntiviral responseInterferon gene expression signatureChronic inflammatory disordersType I interferonCommon gene signaturePeripheral inflammationGene expression signaturesImmune dysregulationChronic inflammationMetabolic decompensationInflammatory disordersInterleukin-1βSymptom progressionT cellsInflammatory signalingMouse modelI interferonMitochondrial diseasePatientsTranslational evidenceMELAS patientsDysfunctionMicrobiota-derived acetate enhances host antiviral response via NLRP3
Niu J, Cui M, Yang X, Li J, Yao Y, Guo Q, Lu A, Qi X, Zhou D, Zhang C, Zhao L, Meng G. Microbiota-derived acetate enhances host antiviral response via NLRP3. Nature Communications 2023, 14: 642. PMID: 36746963, PMCID: PMC9901394, DOI: 10.1038/s41467-023-36323-4.Peer-Reviewed Original ResearchConceptsViral infectionGut-lung axisRespiratory viral infectionsNLRP3-deficient miceIFN-I productionHost immune responsePathogenic viral infectionPotential therapeutic targetType I interferonHost antiviral responseRespiratory virusesIAV infectionMAVS aggregationNLRP3 inflammasomeDeficient miceImmune responseProtective effectTherapeutic targetI interferonGut microbiotaAntiviral responseNLRP3Host defenseInfectionEnhanced induction
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