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.
A combination of genetic fate-mapping and parabiotic experiments reveals the chronological expansion of yolk-sac-derived renal tissue-resident macrophages with age by cellular proliferation and recruitment from circulating progenitors.
Combination of stem cell engineering and CRISPR technologies created a facile method to genetically manipulate macrophages, a multifunctional cell type that plays critical roles in immunity, cancer, and tissue homeostasis.
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.
Measurement of post-translational modifications in primary macrophages infected with Mtb revealed phosphorylation of TAX1BP1, an autophagy receptor that enables full maturation of the Mtb autophagosome.