2023
CXCL8/CXCR2 signaling mediates bone marrow fibrosis and is a therapeutic target in myelofibrosis
Dunbar A, Kim D, Lu M, Farina M, Bowman R, Yang J, Park Y, Karzai A, Xiao W, Zaroogian Z, O’Connor K, Mowla S, Gobbo F, Verachi P, Martelli F, Sarli G, Xia L, Elmansy N, Kleppe M, Chen Z, Xiao Y, McGovern E, Snyder J, Krishnan A, Hill C, Cordner K, Zouak A, Salama M, Yohai J, Tucker E, Chen J, Zhou J, McConnell T, Migliaccio A, Koche R, Rampal R, Fan R, Levine R, Hoffman R. CXCL8/CXCR2 signaling mediates bone marrow fibrosis and is a therapeutic target in myelofibrosis. Blood 2023, 141: 2508-2519. PMID: 36800567, PMCID: PMC10273167, DOI: 10.1182/blood.2022015418.Peer-Reviewed Original ResearchConceptsConstitutive JAK/STATHematopoietic stem/progenitor cellsJAK/STATBone marrow fibrosisStem/progenitor cellsMPN cellsMarrow fibrosisHuman cancersMyeloproliferative neoplasmsPrimary cellsProgenitor cellsMechanistic insightsPharmacologic inhibitionGenetic deletionSignaling contributesGene signatureJAK inhibitor therapyTherapeutic targetingEnhanced proliferationCritical roleTherapeutic targetCXCL8/MF developmentMF pathogenesisInhibitor therapy
2016
AI-22 Single cell protein and transcriptional profiling of CD4+ follicular B helper T (TFH) and central memory (TCM) cells in SLE: physiological and pathological phenotypes
Kwak M, Choi J, Kim S, Chen Z, Lee G, Craft J, Fan R. AI-22 Single cell protein and transcriptional profiling of CD4+ follicular B helper T (TFH) and central memory (TCM) cells in SLE: physiological and pathological phenotypes. Lupus Science & Medicine 2016, 3: a11. DOI: 10.1136/lupus-2016-000179.22.Peer-Reviewed Original ResearchCentral memory cellsTCM cellsTfh cellsSLE patientsHealthy donorsT cellsFollicular B helper T cellsSystemic lupus erythematosusCirculation of patientsHelper T cellsSLE T cellsLupus kidneysHumoral autoimmunityTranscriptional profilingIL-21Lupus erythematosusCytokine producersHelper TMurine lupusHumoral immunityLymphoid organsEnd organsLupus researchPathological outcomesTherapeutic target