Induction of Siglec-FhiCD101hi eosinophils in the lungs following murine hookworm Nippostrongylus brasiliensis infection
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A. Cunningham | M. O’Shea | W. Horsnell | M. Darby | M. Ritter | L. Layland | G. Katawa | Jamie Pillaye | Alisha Chetty | A. Taliep | Matthew G. Darby
[1] Z. Liu,et al. Maturation and specialization of group 2 innate lymphoid cells through the lung-gut axis , 2022, Nature communications.
[2] A. Munitz,et al. Mouse resident lung eosinophils are dependent on IL‐5 , 2022, Allergy.
[3] C. Svanes,et al. Ascaris exposure and its association with lung function, asthma, and DNA methylation in Northern Europe. , 2021, The Journal of allergy and clinical immunology.
[4] B. Ryffel,et al. Il4ra-independent vaginal eosinophil accumulation following helminth infection exacerbates epithelial ulcerative pathology of HSV-2 infection , 2021, Cell host & microbe.
[5] L. Lione,et al. PI3Kδ inhibition prevents IL33, ILC2s and inflammatory eosinophils in persistent airway inflammation , 2021, BMC Immunology.
[6] Jianbo Shi,et al. Elevated Levels of Activated and Pathogenic Eosinophils Characterize Moderate-Severe House Dust Mite Allergic Rhinitis , 2020, Journal of immunology research.
[7] Yin-fang Wu,et al. Homeostatic and early-recruited CD101− eosinophils suppress endotoxin-induced acute lung injury , 2020, European Respiratory Journal.
[8] R. Locksley,et al. Tissue-specific pathways extrude activated ILC2s to disseminate type 2 immunity , 2020, The Journal of experimental medicine.
[9] L. Gregory,et al. Pulmonary Group 2 Innate Lymphoid Cell Phenotype Is Context Specific: Determining the Effect of Strain, Location, and Stimuli , 2020, Frontiers in Immunology.
[10] B. O’Connor,et al. BATF acts as an essential regulator of IL-25–responsive migratory ILC2 cell fate and function , 2020, Science Immunology.
[11] Elisabeth M. Larson,et al. The Prostaglandin D2 Receptor CRTH2 Promotes IL-33–Induced ILC2 Accumulation in the Lung , 2020, The Journal of Immunology.
[12] T. Betsuyaku,et al. Dysregulated fatty acid metabolism in nasal polyp‐derived eosinophils from patients with chronic rhinosinusitis , 2019, Allergy.
[13] N. Beeching,et al. Human Hookworm Infection Enhances Mycobacterial Growth Inhibition and Associates With Reduced Risk of Tuberculosis Infection , 2018, Front. Immunol..
[14] P. Hotez,et al. Ascaris Larval Infection and Lung Invasion Directly Induce Severe Allergic Airway Disease in Mice , 2018, Infection and Immunity.
[15] J. Lasky,et al. A critical role for IL-18 in transformation and maturation of naive eosinophils to pathogenic eosinophils. , 2018, The Journal of allergy and clinical immunology.
[16] P. Fallon,et al. Helminth Modulation of Lung Inflammation. , 2018, Trends in parasitology.
[17] R. Germain,et al. S1P-dependent interorgan trafficking of group 2 innate lymphoid cells supports host defense , 2018, Science.
[18] James J. Lee,et al. SiglecF+Gr1hi eosinophils are a distinct subpopulation within the lungs of allergen‐challenged mice , 2017, Journal of leukocyte biology.
[19] M. Thiry,et al. Lung-resident eosinophils represent a distinct regulatory eosinophil subset. , 2016, The Journal of clinical investigation.
[20] A. Misharin,et al. Phenotypic plasticity and targeting of Siglec‐FhighCD11clow eosinophils to the airway in a murine model of asthma , 2016, Allergy.
[21] T. F. O’Brien,et al. Cytokine expression by invariant natural killer T cells is tightly regulated throughout development and settings of type-2 inflammation , 2015, Mucosal Immunology.
[22] T. Nutman,et al. Eosinophilia in Infectious Diseases. , 2015, Immunology and allergy clinics of North America.
[23] B. Delahunt,et al. ILC2s and T cells cooperate to ensure maintenance of M2 macrophages for lung immunity against hookworms , 2015, Nature Communications.
[24] Xi Chen,et al. IL-25-responsive, lineage-negative KLRG1hi cells are multipotential “inflammatory” type 2 innate lymphoid cells , 2014, Nature Immunology.
[25] R. Maizels,et al. Chitinase-like proteins promote IL-17-mediated neutrophilia in a trade-off between nematode killing and host damage , 2014, Nature Immunology.
[26] Charles C. Kim,et al. Neutrophils prime a long-lived effector macrophage phenotype that mediates accelerated helminth expulsion , 2014, Nature Immunology.
[27] R. Locksley,et al. Type 2 innate lymphoid cells control eosinophil homeostasis , 2013, Nature.
[28] F. Brombacher,et al. Lung-resident CD4+ T cells are sufficient for IL-4Rα-dependent recall immunity to Nippostrongylus brasiliensis infection , 2013, Mucosal Immunology.
[29] Kenji Nakanishi,et al. Contribution of IL-33–activated type II innate lymphoid cells to pulmonary eosinophilia in intestinal nematode-infected mice , 2012, Proceedings of the National Academy of Sciences.
[30] D. Voehringer,et al. Protective immunity against the gastrointestinal nematode Nippostrongylus brasiliensis requires a broad T‐cell receptor repertoire , 2011, Immunology.
[31] David J. Erle,et al. Systemically dispersed innate IL-13–expressing cells in type 2 immunity , 2010, Proceedings of the National Academy of Sciences.
[32] A. McKenzie,et al. Nuocytes represent a new innate effector leukocyte that mediates type-2 immunity , 2010, Nature.
[33] F. Brombacher,et al. Interleukin-4-Promoted T Helper 2 Responses Enhance Nippostrongylus brasiliensis-Induced Pulmonary Pathology , 2008, Infection and Immunity.
[34] M. Kurrer,et al. Nippostrongylus brasiliensis infection leads to the development of emphysema associated with the induction of alternatively activated macrophages , 2008, European journal of immunology.
[35] Niamh E Mangan,et al. Identification of an interleukin (IL)-25–dependent cell population that provides IL-4, IL-5, and IL-13 at the onset of helminth expulsion , 2006, The Journal of experimental medicine.
[36] R. Crystal,et al. Localized Eosinophil Degranulation Mediates Disease in Tropical Pulmonary Eosinophilia , 2003, Infection and Immunity.
[37] L. Proudfoot,et al. Anti‐inflammatory responses and oxidative stress in Nippostrongylus brasiliensis‐induced pulmonary inflammation , 2002, Parasite immunology.
[38] G. Köhler,et al. Eosinophils are not required to induce airway hyperresponsiveness after nematode infection , 1998, European journal of immunology.
[39] F. Finkelman,et al. IL-13, IL-4Ralpha, and Stat6 are required for the expulsion of the gastrointestinal nematode parasite Nippostrongylus brasiliensis. , 1998, Immunity.
[40] R. Coffman,et al. In vivo administration of antibody to interleukin-5 inhibits increased generation of eosinophils and their progenitors in bone marrow of parasitized mice. , 1990, Blood.
[41] F. Brombacher,et al. IL-4Rα-responsive smooth muscle cells contribute to initiation of TH2 immunity and pulmonary pathology in Nippostrongylus brasiliensis infections , 2011, Mucosal Immunology.
[42] K. Kabashima,et al. Immunopathology and Infectious Diseases FTY 720 Regulates Bone Marrow Egress of Eosinophils and Modulates Late-Phase Skin Reaction in Mice , 2010 .