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.

Enriching the interactome with context-specific information from proteomics helps the identification of novel regulators of macrophage activation.

Type 2 cytokines induce macrophage innate training, where enhanced pro-inflammatory responses are fuelled by oxidative phosphorylation rather than aerobic glycolysis.

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.

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.

A mutual information algorithm points to macrophage activation syndrome as a specific pathogenic mechanism in COVID-19, correlated with disease severity, which could be used to monitor disease and therapeutics.

Degradation of kinase LynA protects macrophages from activation unless cells sense a receptor-binding pathogen or inflammation

Activation of lung macrophage nitric oxide synthase-3 improves both bacterial clearance and outcome in primary and secondary pneumonia models.

Direct and selective activation of TRPML2 promotes macrophage migration through release of CCL2.