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.

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.

Obesity leads to increased phosphatidylcholine turnover in adipose tissue macrophages that makes them susceptible to saturated fatty acid-induced inflammation.

Inflammatory dynamics are tailored to bacterial class through macrophage integration of microbial stimuli and cytokine feedback.

Quantifiable bioenergetic parameters, determined from extracellular flux analyses, are distinct between macrophages infected with Mycobacteriumtuberculosis or vaccine strain M. bovis BCG, enabling assessment of future vaccine and drug efficacy.

Vascular degeneration of the choroid and RPE disorganization were associated with pharmacological macrophage ablation, indicating that insufficiency of macrophage function may be a mechanism underlying age- and AMD-associated pathology.

The discovery of evolutionarily conserved macrophage subsets in zebrafish paves the way for a comprehensive study of macrophage behaviour and function.

The anti-tuberculosis drug bedaquiline reprograms human macrophages into potent bactericidal phagocytes, which are able to control bacterial infection.

Macrophage Bmal1 controls the timing of the glycolytic to oxidative metabolism transition that dictates the extent of Hif-1a activation and the associated inflammatory response.

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.