Featured Publications
Co-option of Neutrophil Fates by Tissue Environments
Ballesteros I, Rubio-Ponce A, Genua M, Lusito E, Kwok I, Fernández-Calvo G, Khoyratty TE, van Grinsven E, González-Hernández S, Nicolás-Ávila JÁ, Vicanolo T, Maccataio A, Benguría A, Li JL, Adrover JM, Aroca-Crevillen A, Quintana JA, Martín-Salamanca S, Mayo F, Ascher S, Barbiera G, Soehnlein O, Gunzer M, Ginhoux F, Sánchez-Cabo F, Nistal-Villán E, Schulz C, Dopazo A, Reinhardt C, Udalova IA, Ng LG, Ostuni R, Hidalgo A. Co-option of Neutrophil Fates by Tissue Environments. Cell 2020, 183: 1282-1297.e18. PMID: 33098771, DOI: 10.1016/j.cell.2020.10.003.Peer-Reviewed Original ResearchConceptsNeutrophil fateDepletion of neutrophilsHematopoietic recoveryVascular repairNeutrophil statesNeutrophil propertiesViral infectionNeutrophilsTarget tissuesHealthy tissueGenotoxic injuryEarly ageMultiple tissuesTissueTissue environmentPhysiological demandsInflammationHematopoietic homeostasisCXCR4LungNon-canonical functionsInjuryCancerInfectionLeukocytes
2024
Recruited atypical Ly6G+ macrophages license alveolar regeneration after lung injury
Ruscitti C, Abinet J, Maréchal P, Meunier M, de Meeûs C, Vanneste D, Janssen P, Dourcy M, Thiry M, Bureau F, Schneider C, Machiels B, Hidalgo A, Ginhoux F, Dewals B, Guiot J, Schleich F, Garigliany M, Bellahcène A, Radermecker C, Marichal T. Recruited atypical Ly6G+ macrophages license alveolar regeneration after lung injury. Science Immunology 2024, 9: eado1227-eado1227. PMID: 39093958, PMCID: PMC7616420, DOI: 10.1126/sciimmunol.ado1227.Peer-Reviewed Original ResearchConceptsLung injuryAlveolar regenerationGranulocyte-macrophage colony-stimulating factorColony-stimulating factorType 2 epithelial cellsAlveolar type 2 epithelial cellsPopulation of macrophagesModels of injuryImmune cellsSuspected pneumoniaA virusAlveolar damageEpithelial regenerationInterleukin-4Lung damageMacrophage subsetsReceptor signalingLungPerilesional areaRepair responseMacrophagesTherapeutic targetInjuryCellsAirborne pathogens
2020
Programmed ‘disarming’ of the neutrophil proteome reduces the magnitude of inflammation
Adrover JM, Aroca-Crevillén A, Crainiciuc G, Ostos F, Rojas-Vega Y, Rubio-Ponce A, Cilloniz C, Bonzón-Kulichenko E, Calvo E, Rico D, Moro MA, Weber C, Lizasoaín I, Torres A, Ruiz-Cabello J, Vázquez J, Hidalgo A. Programmed ‘disarming’ of the neutrophil proteome reduces the magnitude of inflammation. Nature Immunology 2020, 21: 135-144. PMID: 31932813, PMCID: PMC7223223, DOI: 10.1038/s41590-019-0571-2.Peer-Reviewed Original ResearchConceptsMagnitude of inflammationNeutrophil extracellular trapsNeutrophil proteomeGranule contentsInflammatory injuryRespiratory distressPneumonia patientsExtracellular trapsCell-intrinsic programsProgressive lossHuman neutrophilsNET formationProtein storesNeutrophilsInflammationLungAntimicrobial functionMouse mutantsCircadian cyclePatientsInjuryTime of dayArmamentariumIncidenceSeverity
2014
Neutrophils scan for activated platelets to initiate inflammation
Sreeramkumar V, Adrover JM, Ballesteros I, Cuartero MI, Rossaint J, Bilbao I, Nácher M, Pitaval C, Radovanovic I, Fukui Y, McEver RP, Filippi MD, Lizasoain I, Ruiz-Cabello J, Zarbock A, Moro MA, Hidalgo A. Neutrophils scan for activated platelets to initiate inflammation. Science 2014, 346: 1234-1238. PMID: 25477463, PMCID: PMC4280847, DOI: 10.1126/science.1256478.Peer-Reviewed Original Research
2009
Heterotypic interactions enabled by polarized neutrophil microdomains mediate thromboinflammatory injury
Hidalgo A, Chang J, Jang JE, Peired AJ, Chiang EY, Frenette PS. Heterotypic interactions enabled by polarized neutrophil microdomains mediate thromboinflammatory injury. Nature Medicine 2009, 15: 384-391. PMID: 19305412, PMCID: PMC2772164, DOI: 10.1038/nm.1939.Peer-Reviewed Original Research