Kishu Ranjan, PhD
Associate Research Scientist in PathologyCards
About
Research
Publications
Featured Publications
IL-4 mediated TAP2 downregulation is a dominant and reversible mechanism of immune evasion and immunotherapy resistance in non-small cell lung cancer
Ranjan K, Rajendran B, Deen I, Costantini A, de Rodas M, Desai S, Scallo F, Gianino N, Ferrone S, Schalper K. IL-4 mediated TAP2 downregulation is a dominant and reversible mechanism of immune evasion and immunotherapy resistance in non-small cell lung cancer. Molecular Cancer 2025, 24: 80. PMID: 40091029, PMCID: PMC11912681, DOI: 10.1186/s12943-025-02276-z.Peer-Reviewed Original ResearchThis study investigates IL-4's role in TAP2 downregulation as a reversible mechanism of immune evasion and resistance to immunotherapy in non-small cell lung cancer, highlighting potential therapeutic strategies to restore TAP2 expression and enhance treatment efficacy.Ubiquitination of ATF6 by disease-associated RNF186 promotes the innate receptor-induced unfolded protein response
Ranjan K, Hedl M, Sinha S, Zhang X, Abraham C. Ubiquitination of ATF6 by disease-associated RNF186 promotes the innate receptor-induced unfolded protein response. Journal Of Clinical Investigation 2021, 131: e145472. PMID: 34623328, PMCID: PMC8409591, DOI: 10.1172/jci145472.Peer-Reviewed Original ResearchMeSH KeywordsActivating Transcription Factor 6AnimalsEndoplasmic Reticulum StressGenetic VariationHost Microbial InteractionsHumansImmunity, InnateInflammatory Bowel DiseasesMacrophagesMiceMice, Inbred C57BLMice, KnockoutNod2 Signaling Adaptor ProteinReceptors, Pattern RecognitionRisk FactorsSignal TransductionUbiquitin-Protein LigasesUbiquitinationUnfolded Protein ResponseConceptsPattern recognition receptorsUnfolded protein responseInflammatory bowel diseaseER stress sensorsHuman macrophagesIntestinal immune homeostasisProtein responseInnate immune systemRisk variantsKey macrophage functionsBowel diseaseOral challengeTranscription factor 6Immune homeostasisCytokine secretionColonic tissueMacrophage functionStress sensorImmune systemRecognition receptorsEffective clearanceMicrobial responsesWeight lossMacrophagesUbiquitinationThe E3 ubiquitin ligase RNF186 and RNF186 risk variants regulate innate receptor-induced outcomes
Ranjan K, Hedl M, Abraham C. The E3 ubiquitin ligase RNF186 and RNF186 risk variants regulate innate receptor-induced outcomes. Proceedings Of The National Academy Of Sciences Of The United States Of America 2021, 118: e2013500118. PMID: 34353900, PMCID: PMC8364215, DOI: 10.1073/pnas.2013500118.Peer-Reviewed Original ResearchMeSH KeywordsCytokinesHumansImmunity, InnateInflammatory Bowel DiseasesIntestinesMacrophagesMyeloid CellsNF-kappa BNod2 Signaling Adaptor ProteinPolymorphism, Single NucleotideReceptor-Interacting Protein Serine-Threonine Kinase 2Receptors, Pattern RecognitionToll-Like Receptor 2Toll-Like Receptor 4Ubiquitin-Protein LigasesUbiquitinationConceptsPattern recognition receptorsE3 ubiquitin ligase activityStimulation of PRRsAntimicrobial reactive oxygen speciesMultiple pattern recognition receptorsLoss of functionLigase activityReactive nitrogen speciesComplex assemblyIntestinal myeloid cellsReactive oxygen speciesAutophagy pathwayDownstream signalingRNF186Bacterial clearanceRisk variantsRecognition receptorsHuman macrophagesOxygen speciesInnate immunityInflammatory bowel diseaseNitrogen speciesMicrobial clearanceSpeciesMyeloid cellsMyeloid Cell Expression of LACC1 Is Required for Bacterial Clearance and Control of Intestinal Inflammation
Kang JW, Yan J, Ranjan K, Zhang X, Turner JR, Abraham C. Myeloid Cell Expression of LACC1 Is Required for Bacterial Clearance and Control of Intestinal Inflammation. Gastroenterology 2020, 159: 1051-1067. PMID: 32693188, PMCID: PMC8139320, DOI: 10.1053/j.gastro.2020.07.024.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCD4-Positive T-LymphocytesCells, CulturedCoculture TechniquesColitis, UlcerativeCytokinesDextran SulfateDisease Models, AnimalDNA-Binding ProteinsFemaleHost Microbial InteractionsHumansImmunity, MucosalIntestinal MucosaIntracellular Signaling Peptides and ProteinsMaleMiceMice, KnockoutMyeloid CellsPrimary Cell CultureSalmonella InfectionsSalmonella typhimuriumConceptsIntestinal lymphoid organsBurden of bacteriaDextran sodium sulfateWild-type miceLymphoid organsTh17 cytokinesIntestinal inflammationDendritic cellsMyeloid cellsT cellsTh2 cytokinesMesenteric lymph node dendritic cellsLymph node dendritic cellsMyeloid cell-derived cytokinesAdaptive T cell responsesT cell transfer colitisMyeloid-specific disruptionInflammatory bowel diseaseReactive oxygen speciesImmune-mediated diseasesT cell responsesT helper 1Cell-derived cytokinesT cell cytokinesBone marrow-derived macrophagesLACC1 Required for NOD2-Induced, ER Stress-Mediated Innate Immune Outcomes in Human Macrophages and LACC1 Risk Variants Modulate These Outcomes
Huang C, Hedl M, Ranjan K, Abraham C. LACC1 Required for NOD2-Induced, ER Stress-Mediated Innate Immune Outcomes in Human Macrophages and LACC1 Risk Variants Modulate These Outcomes. Cell Reports 2019, 29: 4525-4539.e4. PMID: 31875558, PMCID: PMC7372507, DOI: 10.1016/j.celrep.2019.11.105.Peer-Reviewed Original ResearchMeSH KeywordsActivating Transcription Factor 6eIF-2 KinaseEndoplasmic ReticulumEndoplasmic Reticulum StressEndoribonucleasesEnterococcus faecalisEscherichia coliGene Expression RegulationHeLa CellsHost-Pathogen InteractionsHumansImmunity, InnateIntracellular Signaling Peptides and ProteinsMacrophagesNod2 Signaling Adaptor ProteinPhagocytosisPrimary Cell CultureProtein Serine-Threonine KinasesRiskSignal TransductionConceptsEndoplasmic reticulumER stressER stress sensorsHuman macrophagesInnate immune outcomesDisease risk variantsMultiple immune-mediated diseasesLaccase domainPattern recognition receptor NOD2HeLa cellsAntimicrobial pathwaysRisk variantsGenetic variantsLACC1Critical roleVariantsMacrophagesATF6IRE1αArg284SignalingReticulumStressTransfectionPERKFADD regulates NF-κB activation and promotes ubiquitination of cFLIPL to induce apoptosis
Ranjan K, Pathak C. FADD regulates NF-κB activation and promotes ubiquitination of cFLIPL to induce apoptosis. Scientific Reports 2016, 6: 22787. PMID: 26972597, PMCID: PMC4789601, DOI: 10.1038/srep22787.Peer-Reviewed Original ResearchMeSH KeywordsA549 CellsAnimalsApoptosisBaculoviral IAP Repeat-Containing 3 ProteinBlotting, WesternCASP8 and FADD-Like Apoptosis Regulating ProteinCaspase 8Cell LineCell SurvivalFas-Associated Death Domain ProteinHCT116 CellsHEK293 CellsHeLa CellsHT29 CellsHumansInhibitor of Apoptosis ProteinsMCF-7 CellsMiceNF-kappa BNIH 3T3 CellsProtein BindingRepressor ProteinsRNA InterferenceTumor Necrosis Factor-alphaUbiquitin-Protein LigasesUbiquitinationConceptsCell deathProcaspase-8Molecular mechanismsCellular FLICE-like inhibitory proteinFLICE-like inhibitory proteinExpression of cFLIPLCell death signalingApoptosis protein 2Apoptotic cell death signalingHEK 293T cellsNovel molecular mechanismApoptotic cell deathNF-κB activationFasL stimulationCellular inhibitorE3 ubiquitinTNF-α stimulationDeath domainDeath inducingDeath signalingEctopic expressionFADDCaspase-8NF-κBCell survival
2026
NSCLC brain metastases exhibit reduced HLA-I antigen presentation machinery and immune evasion independent of IFNγ signaling defects.
Vilariño N, de Rodas ML, Villalba-Esparza M, Rajendran BK, Huang B, Hijazo-Pechero S, Costantini A, Ranjan K, Ramos-Paradas J, Lu BY, Nadal E, Goldberg SB, Nguyen DX, Schalper KA. NSCLC brain metastases exhibit reduced HLA-I antigen presentation machinery and immune evasion independent of IFNγ signaling defects. Mol Cancer 2026 PMID: 42210261, DOI: 10.1186/s12943-026-02687-6.Peer-Reviewed Original Research
2025
Molecular Perspective on Proteases: Regulation of Programmed Cell Death Signaling, Inflammation and Pathological Outcomes
Ansari A, Ranjan K, Kumar A, Pathak C. Molecular Perspective on Proteases: Regulation of Programmed Cell Death Signaling, Inflammation and Pathological Outcomes. Journal Of Molecular Pathology 2025, 6: 32. DOI: 10.3390/jmp6040032.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsProgrammed cell death signalingCell deathCellular signaling networksCell death signalingModality of cell deathDownstream signal transduction pathwaysSignal transduction pathwaysResponse to pathogenGroup of proteasesActivity of proteinsImmune response to pathogenDeath signalingSignaling networksCellular fateCellular signalingTransduction pathwaysCell growthHuman diseasesPotential therapeutic targetSignaling mechanismsPhysiological processesProteasePhysiological functionsPeptide bondDisease pathogenesisTumor microenvironment of non-small cell lung cancer impairs immune cell function among people with HIV
Desai S, Salahuddin S, Yusuf R, Ranjan K, Gu J, Osmani L, Lin Y, Mehta S, Talmon R, Kang I, Kluger Y, Zhao H, Schalper K, Emu B. Tumor microenvironment of non-small cell lung cancer impairs immune cell function among people with HIV. Journal Of Clinical Investigation 2025, 135: e177310. PMID: 40459946, PMCID: PMC12259253, DOI: 10.1172/jci177310.Peer-Reviewed Original ResearchNon-small cell lung cancerTumor microenvironmentImmune cellsLung cancerCohort of non-small cell lung cancerExpression of PD-1Impairs anti-tumor responsesTumor-infiltrating CD8+Tumor-specific immune responsesCD4+ T cellsHIV-associated tumorsInfiltrating CD8+Expression of immunoregulatory moleculesAnti-tumor responsesTumor-associated macrophagesCell lung cancerImmune cell functionNSCLC cell linesPD-1Tumor killingBlocker therapyCD8+LAG-3Immune landscapeImmunoregulatory phenotypeEmerging Concept of Receptor Endocytosis and Signaling
Kumar A, Panda A, Kumar S, Ranjan K. Emerging Concept of Receptor Endocytosis and Signaling. The Receptors 2025, 2: 61-84. DOI: 10.1007/978-3-031-81991-9_3.ChaptersReceptor endocytosisMaintenance of cell polarityRegulation of receptor internalizationRare human diseasesInternalization of ligand-receptor complexesMechanisms of endocytosisIntracellular signal transductionEndocytic adaptorsMembrane lipid compositionReceptor sortingEndocytic signalEndocytosis signalCell polarityCellular processesEndocytic mechanismsSignal transductionKinase proteinLigand-receptor complexesHuman diseasesEndocytosisEssential functionReceptor internalizationCellular environmentNutrient uptakeIntracellular mechanisms
Academic Achievements & Community Involvement
News & Links
News
- June 24, 2026
Award to Support Ranjan’s Research on Non-Small Cell Lung Cancer
- January 18, 2023
Resistance to immune checkpoint inhibitors in NSCLC
- December 01, 2022Source: Bioanalysis Zone
COVID-19 variants and cell and gene therapies – panel discussion
- November 28, 2022Source: VuMedi
SITC 2022: TAP2 Deficiency Mediates Adaptive Immune Evasion and Immunotherapy Resistance in Human NSCLC
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