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    1. Cell Biology
    2. Microbiology and Infectious Disease

    Tuberculosis-associated IFN-I induces Siglec-1 on tunneling nanotubes and favors HIV-1 spread in macrophages

    Maeva Dupont et al.
    Type-I interferon enriched microenvironment generated by Mycobacterium tuberculosis induces the Siglec-1 receptor expression in human macrophages, including on tunneling nanotubes, and contributes to the exacerbation of cell-to-cell transfer of HIV-1.
    1. Immunology and Inflammation

    MicroRNAs of the miR-17~92 family maintain adipose tissue macrophage homeostasis by sustaining IL-10 expression

    Xiang Zhang et al.
    miR-17~92 family of miRNAs control the balance between pro- and anti-inflammatory cytokines in adipose tissue macrophages, the absence of which leads to disturbed adipose homeostasis.
    1. Developmental Biology

    EKLF/KLF1 expression defines a unique macrophage subset during mouse erythropoiesis

    Kaustav Mukherjee et al.
    Mouse fetal liver macrophages that support erythroid differentiation within erythroblastic islands exhibit a unique and transient expression signature under transcriptional control of EKLF/KLF1.
    1. Immunology and Inflammation

    A type I IFN-dependent DNA damage response regulates the genetic program and inflammasome activation in macrophages

    Abigail J Morales et al.
    Activated macrophages initiate a robust DNA damage response that depends on type I IFN and regulates their genetic program and inflammasome activation, establishing a mechanistic link between DNA damage responses and innate immunity.
    1. Chromosomes and Gene Expression
    2. Immunology and Inflammation

    Gene-specific mechanisms direct glucocorticoid-receptor-driven repression of inflammatory response genes in macrophages

    Maria A Sacta et al.
    A comprehensive analysis of the glucocorticoid-sensitive pro-inflammatory genes in macrophages reveals fundamental differences between the temporal events and components of transcriptional machinery that the glucocorticoid receptor targets to repress their transcription.
    1. Immunology and Inflammation

    Drosophila macrophages switch to aerobic glycolysis to mount effective antibacterial defense

    Gabriela Krejčová et al.
    Activated Drosophila macrophages undergo transient metabolic remodeling towards Hypoxia inducible factor 1 α-driven aerobic glycolysis, a program that induces systemic metabolic changes and is crucial for resistance to infection.
    1. Cancer Biology
    2. Immunology and Inflammation

    Tumor initiating cells induce Cxcr4-mediated infiltration of pro-tumoral macrophages into the brain

    Kelda Chia et al.
    Pre-neoplastic cells in the brain release SDF1, which mediates an immediate infiltration of macrophages that differentiate into microglia-like cells and promote proliferation of pre-neoplastic cells.
    1. Computational and Systems Biology
    2. Microbiology and Infectious Disease

    Intracellular growth of Mycobacterium tuberculosis after macrophage cell death leads to serial killing of host cells

    Deeqa Mahamed et al.
    The rapid killing of macrophages by Mycobacterium tuberculosis aggregates, and the subsequent proliferation of the bacteria inside the dead cell, leads to a cell death cascade and explains the coupling of necrosis and pathogen growth observed in active disease.
    1. Immunology and Inflammation

    Yolk-sac-derived macrophages progressively expand in the mouse kidney with age

    Shintaro Ide et al.
    A combination of genetic fate-mapping and parabiotic experiments reveals the chronological expansion of yolk-sac-derived renal tissue-resident macrophages with age by cellular proliferation and recruitment from circulating progenitors.
    1. Immunology and Inflammation

    Macrophage dysfunction initiates colitis during weaning of infant mice lacking the interleukin-10 receptor

    Naresh S Redhu et al.
    A detailed time-series analysis reveals that the interleukin-10 receptor prevents susceptibility to microbiota-driven colonic inflammation that emerges at the time of weaning by directly inhibiting the acquisition of a pro-inflammatory intestinal macrophage phenotype.