The thioredoxin-1 (Trx1) system promotes inflammation by positively regulating both NLRP3 inflammasome responses, by detoxifying excessive ROS independently of Txnip and NF-κB binding to target DNA.

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 genetic screen in combination with biochemical approaches reveal hijacking of the host β-catenin destruction complex by the parasite T. gondii to reprogram immune gene expression.

Decay rate of mRNAs encoding inflammatory regulators is controlled by the balance between AU-rich element-mediated deadenylation and cytoplasmic polyadenylation element-mediated polyadenylation.

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

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

Transcriptomic and bionergetic analysis shows the importance of HIF-1α activation in enabling tissue-resident alveolar macrophages to perform glycolytic metabolism, which prevents their death and attenuates influenza A virus-induced acute lung injury.

Biochemical and microscopy-based approaches in mouse and human macrophages reveal that glycine cytoprotection acts at the level of the newly identified pan-death protein NINJ1 to inhibit multiple lytic cell death pathways, thereby resolving a long-standing mechanism of glycine cytoprotection.

Zinc transporter Slc30a1 mediates antibacterial defense in macrophages.

Chromosomal instability induced in solid tumors can combine with macrophages that are made highly phagocytic to thereby initiate elimination of and immunity against poorly immunogenic tumors in immunocompetent mice.