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.

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.

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

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.