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.

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.

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.

An unbiased forward genetic screen identified genes in Mycobacterium tuberculosis that are required for fatty acid import when the bacterium is residing within macrophages.

Autocrine activation of macrophages is modulated by Connexin-43-mediated ATP release in response to TLR-4 and -2 agonists in a P2Y1-dependent manner, ultimately determining sepsis survival.