2024
KLF13 promotes SLE pathogenesis by modifying chromatin accessibility of key proinflammatory cytokine genes
Wang A, Fairhurst A, Liu K, Wakeland B, Barnes S, Malladi V, Viswanathan K, Arana C, Dozmorov I, Singhar A, Du Y, Imam M, Moses A, Chen C, Sunkavalli A, Casco J, Rakheja D, Li Q, Mohan C, Clayberger C, Wakeland E, Khan S. KLF13 promotes SLE pathogenesis by modifying chromatin accessibility of key proinflammatory cytokine genes. Communications Biology 2024, 7: 1446. PMID: 39506084, PMCID: PMC11541912, DOI: 10.1038/s42003-024-07099-0.Peer-Reviewed Original ResearchConceptsSystemic lupus erythematosusMyeloid cellsLupus nephritisT cellsKidneys of lupus-prone miceSystemic lupus erythematosus pathogenesisLevels of proinflammatory cytokinesLupus-prone miceActivated myeloid cellsActivated T cellsT cell activationProduction of RANTEST cell hyperactivityProinflammatory cytokine genesAssociated with increased productionLupus pathogenesisProinflammatory cytokines/chemokinesSle1 locusLupus erythematosusImmune activationProinflammatory cytokinesCytokine signaling pathwaysCytokine genesGenome-wide transcriptional changesReceptor ligands
2022
Dickkopf1 fuels inflammatory cytokine responses
Jaschke N, Pählig S, Sinha A, Adolph T, Colunga M, Hofmann M, Wang A, Thiele S, Schwärzler J, Kleymann A, Gentzel M, Tilg H, Wielockx B, Hofbauer L, Rauner M, Göbel A, Rachner T. Dickkopf1 fuels inflammatory cytokine responses. Communications Biology 2022, 5: 1391. PMID: 36539532, PMCID: PMC9765382, DOI: 10.1038/s42003-022-04368-8.Peer-Reviewed Original ResearchConceptsInflammatory cytokine responseCytokine responsesCell-autonomous functionCell-autonomous mechanismsElevated cytokine productionMolecular underpinningsNon-malignant cellsCytokine receptorsHuman diseasesPharmacological neutralizationInflammatory toneInflammatory componentCytokine productionCancer cellsGenetic deletionInflammatory responseRelA activityDKK1Mouse modelDisease trajectoriesHealthy populationCell modelAdditional studiesInflammationCells
2020
Origin and Function of Stress-Induced IL-6 in Murine Models
Qing H, Desrouleaux R, Israni-Winger K, Mineur YS, Fogelman N, Zhang C, Rashed S, Palm NW, Sinha R, Picciotto MR, Perry RJ, Wang A. Origin and Function of Stress-Induced IL-6 in Murine Models. Cell 2020, 182: 372-387.e14. PMID: 32610084, PMCID: PMC7384974, DOI: 10.1016/j.cell.2020.05.054.Peer-Reviewed Original ResearchMeSH KeywordsAdipose Tissue, BrownAnimalsBone Marrow CellsBone Marrow TransplantationBrainChemokinesCytokinesDisease Models, AnimalGluconeogenesisHyperglycemiaInterleukin-6LiverMaleMiceMice, Inbred C57BLMice, KnockoutReceptors, Adrenergic, beta-3Receptors, Interleukin-6Stress, PsychologicalUncoupling Protein 1ConceptsInterleukin-6Subsequent inflammatory challengeAcute psychological stressBrown adipose tissueDominant cytokineImmunometabolic reprogrammingInflammatory challengeEndocrine organMurine modelMouse modelAdipose tissueNeuropsychiatric diseasesAcute stressHepatic gluconeogenesisStress hormonesBrown adipocytesPsychological stressDependent fashionDiseaseInstructive signalsHyperglycemiaInflammationCytokinesMortalityHormone
2019
Specific sequences of infectious challenge lead to secondary hemophagocytic lymphohistiocytosis-like disease in mice
Wang A, Pope SD, Weinstein JS, Yu S, Zhang C, Booth CJ, Medzhitov R. Specific sequences of infectious challenge lead to secondary hemophagocytic lymphohistiocytosis-like disease in mice. Proceedings Of The National Academy Of Sciences Of The United States Of America 2019, 116: 2200-2209. PMID: 30674681, PMCID: PMC6369774, DOI: 10.1073/pnas.1820704116.Peer-Reviewed Original ResearchConceptsSecondary hemophagocytic lymphohistiocytosisAssociated transcriptional programRNA sequencing analysisBone marrow-derived macrophagesTranscriptional programsTranscriptional profilingMarrow-derived macrophagesBone marrow macrophagesTranscriptional profilesNonlethal doseMitochondrial functionToll-like receptor agonistsSequencing analysisSpecific sequencesSetting of infectionGlycolytic metabolismMarrow macrophagesUseful therapeutic strategyGlycolysis inhibitorLethal stateHyperinflammatory stateHyperinflammatory responseOxidative metabolismHemophagocytic lymphohistiocytosisMortal complications
2009
CXCR4/CXCL12 Hyperexpression Plays a Pivotal Role in the Pathogenesis of Lupus
Wang A, Fairhurst AM, Tus K, Subramanian S, Liu Y, Lin F, Igarashi P, Zhou XJ, Batteux F, Wong D, Wakeland EK, Mohan C. CXCR4/CXCL12 Hyperexpression Plays a Pivotal Role in the Pathogenesis of Lupus. The Journal Of Immunology 2009, 182: 4448-4458. PMID: 19299746, PMCID: PMC2946082, DOI: 10.4049/jimmunol.0801920.Peer-Reviewed Original ResearchConceptsMurine modelIncreased CXCR4 expressionPathogenesis of lupusB cell subsetsPromising therapeutic targetCXCR4/CXCL12Multiple murine modelsB cell survivalLupus nephritisActive nephritisSerum autoantibodiesCell subsetsCXCR4 expressionInflammatory cytokinesNephritic kidneysOrgan diseasePathogenic rolePlasma cellsLeukocyte traffickingTherapeutic targetLupusPeptide antagonistCXCR4Surface moleculesNephritis