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The lung environment controls alveolar macrophage metabolism and responsiveness during type-2 inflammation.
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Immune Response to Nippostrongylus brasiliensis in the mouse lung
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Lung immune response to Nippostrongylus brasiliensis infection: time course
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Neutrophils promote M2 polarization of macrophages during Nippostrongylus brasiliensis infection
Analysis of tissue-derived alveolar and monocyte-derived alveolar macrophages at day 7 and day 14 post-nippostrongylus brasiliensis infection.
Lung macrophages mediate helminth resistance through differential activation of recruited monocyte-derived alveolar macrophages and arginine depletion
RELMa induced differential gene expression in CD11c+ cells
Transcriptome mapping of alveolar macrophages developing under Scgb1a1 deficiency.
Gene expression profiling of mouse macrophages following long noncoding RNA Malat1 knockdown
The JMJD3-IRF4 axis regulates M2 macrophage polarization and host responses against helminth infection
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Genome wide trimethyl-H3K27 distibution in macrophages from wild-type and Jmjd3-/- macrophages.
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Expression data of LPS-stimulated bone marrow macrophages induced by M-CSF from wild-type and Jmjd3-/- mice.
Specification of innate type-2 lymphocytes by the transcriptional determinant Gfi1
Mouse ILC2 cells from wild-type or Gfi1-KO animals
Human resistin alters lung mRNA expression from helminth-infected lungs.
Hookworm-Induced Persistent Changes to the Immunological Environment of the Lung
Tissue-specific differences in PPARγ control of macrophage function.
Macrophage function in tissue repair and remodeling requires IL-4/IL-13 with apoptotic cells
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Macrophage function in tissue repair and remodeling requires IL-4/IL-13 with apoptotic cells [Run2]
Macrophage function in tissue repair and remodeling requires IL-4/IL-13 with apoptotic cells [Run1]
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