2024
EGFR-Driven Lung Adenocarcinomas Co-opt Alveolar Macrophage Metabolism and Function to Support EGFR Signaling and Growth.
Kuhlmann-Hogan A, Cordes T, Xu Z, Kuna R, Traina K, Robles-Oteíza C, Ayeni D, Kwong E, Levy S, Globig A, Nobari M, Cheng G, Leibel S, Homer R, Shaw R, Metallo C, Politi K, Kaech S. EGFR-Driven Lung Adenocarcinomas Co-opt Alveolar Macrophage Metabolism and Function to Support EGFR Signaling and Growth. Cancer Discovery 2024, of1-of22. PMID: 38270272, DOI: 10.1158/2159-8290.cd-23-0434.Peer-Reviewed Original ResearchLung adenocarcinomaGM-CSFEGFR-mutant lung adenocarcinomaT cell-based immunotherapyTransformed epitheliumOncogenic signalingGM-CSF secretionProinflammatory immune responseSuppress tumor progressionLocal immunosuppressionStatin therapyTherapeutic combinationsNovel therapiesTumor cellsTumor progressionTumor growthLung cancerLung adenocarcinoma cellsEGFR phosphorylationImmune responseImmunological supportCancer cellsInflammatory functionsAlveolar macrophagesIncreased cholesterol synthesisEGFR-driven lung adenocarcinomas coopt alveolar macrophage metabolism and function to support EGFR signaling and growth.
Kuhlmann-Hogan A, Cordes T, Xu Z, Kuna R, Traina K, Robles-Oteiza C, Ayeni D, Kwong E, Levy S, Globig A, Nobari M, Cheng G, Leibel S, Homer R, Shaw R, Metallo C, Politi K, Kaech S. EGFR-driven lung adenocarcinomas coopt alveolar macrophage metabolism and function to support EGFR signaling and growth. Cancer Discovery 2024, 14: 524-545. PMID: 38241033, PMCID: PMC11258210, DOI: 10.1158/2159-8290.cd-23-0434.Peer-Reviewed Original ResearchLung adenocarcinomaGM-CSFEGFR-mutant lung adenocarcinomaGM-CSF secretionProinflammatory immune responseSuppress tumor progressionLocal immunosuppressionStatin therapyTherapeutic combinationsNovel therapiesTumor cellsTumor progressionTumor growthLung adenocarcinoma cellsEGFR phosphorylationImmune responseTransformed epitheliumCancer cellsInflammatory functionsEGFR SignalingMacrophage metabolismAlveolar macrophagesIncreased cholesterol synthesisMetabolic supportOncogenic signaling
2021
Emerging roles of Dectin-1 in noninfectious settings and in the CNS
Deerhake ME, Shinohara ML. Emerging roles of Dectin-1 in noninfectious settings and in the CNS. Trends In Immunology 2021, 42: 891-903. PMID: 34489167, PMCID: PMC8487984, DOI: 10.1016/j.it.2021.08.005.Peer-Reviewed Original ResearchConceptsC-type lectin receptorsImmune responseProinflammatory immune responseCentral nervous systemNew therapeutic approachesInnate immune responseMammalian myeloid cellsNeuroprotective responseSterile inflammationNeurologic disordersTherapeutic approachesNervous systemMyeloid cellsFungal infectionsLectin receptorsRecent studiesCurrent understandingResponseInflammationΒ-glucanInfectionSettingImmunologyReceptors
2015
Bimodal Influence of Vitamin D in Host Response to Systemic Candida Infection—Vitamin D Dose Matters
Lim JH, Ravikumar S, Wang YM, Thamboo TP, Ong L, Chen J, Goh JG, Tay SH, Chengchen L, Win MS, Leong W, Lau T, Foo R, Mirza H, Tan KS, Sethi S, Khoo AL, Chng WJ, Osato M, Netea MG, Wang Y, Chai LY. Bimodal Influence of Vitamin D in Host Response to Systemic Candida Infection—Vitamin D Dose Matters. The Journal Of Infectious Diseases 2015, 212: 635-644. PMID: 25612733, DOI: 10.1093/infdis/jiv033.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCandidiasisCholecalciferolCohort StudiesDose-Response Relationship, DrugGene Expression RegulationHumansInflammationInterferon-gammaLeukocytes, MononuclearMiceMice, Inbred BALB CPromoter Regions, GeneticRNA, MessengerSTAT Transcription FactorsSuppressor of Cytokine Signaling 3 ProteinSuppressor of Cytokine Signaling ProteinsVitamin DConceptsVitamin D levelsCandida infectionsVitamin DD levelsVitamin D3 dosesVitamin D3 supplementationProinflammatory immune responseSystemic Candida infectionSuppression of SOCS3Vitamin D receptorVitamin D response elementD response elementCandidemic patientsD3 supplementationUntreated micePoor outcomeAntiinflammatory effectsFungal burdenVitamin D3Immune responseInterferon γD receptorBetter survivalDose matterBimodal influence
2006
Innate Immunity in Multiple Sclerosis: Myeloid Dendritic Cells in Secondary Progressive Multiple Sclerosis Are Activated and Drive a Proinflammatory Immune Response
Karni A, Abraham M, Monsonego A, Cai G, Freeman GJ, Hafler D, Khoury SJ, Weiner HL. Innate Immunity in Multiple Sclerosis: Myeloid Dendritic Cells in Secondary Progressive Multiple Sclerosis Are Activated and Drive a Proinflammatory Immune Response. The Journal Of Immunology 2006, 177: 4196-4202. PMID: 16951385, DOI: 10.4049/jimmunol.177.6.4196.Peer-Reviewed Original ResearchConceptsMyeloid dendritic cellsDendritic cellsMultiple sclerosisInnate immune systemRR-MSImmune responseImmune systemT cell-mediated autoimmune diseaseSecondary progressive multiple sclerosisCell-mediated autoimmune diseaseStages of MSIncreased percentageProgressive phaseNeuronal degenerative changesSecondary progressive phaseSP-MS patientsProgressive multiple sclerosisProinflammatory immune responsePrimary immune responseNaive T cellsImmunologic basisTh1 responseClinical patternMS patientsPD-L1
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