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.

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

Tissue-resident macrophages sense environmental cues and regulate adaptive immunity via an immune checkpoint molecule CRIg.

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.

Mechanistic insights show how treatment with apoA1 is anti-inflammatory by rapidly disrupting macrophage chemotaxis and monocyte recruitment.

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.

Interleukin 4 signaling co-opts the Akt-mTORC1-Acly pathway to couple metabolic input to the control of energetically demanding processes during macrophage M2 activation.

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.

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.

A new type of skin perivascular macrophages with extramedullary origin, access to blood and exclusive anti-inflammatory reparative properties has been characterized.