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NF-κB oscillations synchronize to external perturbations as a damped oscillator, producing different transcription dynamics.

HOIL-1 deficiency in mice results in a severe immunodeficiency that is effectively complemented by chronic infection with a murine gamma-herpesvirus.

Chronic and excessive inflammation can lead to exhaustion of the supply of hematopoietic stem cells and to myeloid malignancies in mice, mimicking important aspects of the myelodysplastic syndrome found in humans.

Type I interferon signaling protects cells from the loss of epigenetic integrity, since it is activated in cells in response to accumulation of transcripts originating from normally silenced heterochromatin, caused by small-molecule-mediated nucleosome unfolding.

A model of early postnatal bacterial meningitis in the mouse demonstrates the transcriptome responses of each of the major meningeal cell types and should prove useful in dissecting the pathophysiology of bacterial meningitis in human infants.

The neutral amino acid transporter SLC38A2 is an essential protective factor for renal medulla during urine concentration.

Vangl2 induced by inflammation recruits ubiquitin ligase PDLIM2 and increases K63-linked ubiquitination on p65, which promotes the recognition of p65 by cargo receptor NDP52 and the autophagic degradation of p65.

Evidence is provided suggesting that heterochromatin re-organisation during cell senescence can compromise the structural integrity of the nucleus, leading to activation of an inflammatory process.

Contact with bacteria and subsequent hypoxia promotes functional maturation of the immature gastrointestinal tract.

A novel bacterial protease activated by a eukaryote-specific factor attacks a host protein involved in cytoskeleton organization to inhibit cell migration during Legionella pneumophila infection.