Sepsis leads to lasting changes in the composition of the pre-existing memory CD8 T cell compartment leading to altered localization, changes in their transcriptional landscape and chromatin accessibility, differential function, and reduced capacity to control infection.

Long non-coding RNA profiles as a source of signal in sepsis.

Integrative multi-omics reveals global dysregulation in hepatic metabolism during prolonged sepsis.

Imaging with electron microscopy and cryo-electron tomography reveals that competition between Cdc42 and Gic1 for the same subunit within septins controls the formation and breakdown of septin filaments.

Single-cell RNA-sequencing identifies the precise cellular and molecular events that occur along the sepsis timeline in the kidney, pointing to potential biomarkers and therapeutic targets.

A rigorous and transparent evaluation of mesenchymal stem cell therapy for sepsis suggests it may be efficacious, although the strength of these findings is tempered by threats to validity in the studies that were included.

Heparan sulfates in the vessel wall bind and regulate signaling from the megakaryocyte/platelet-specific inhibitory receptor G6b-B, a critical regulator of platelet homeostasis.

A murine model of sepsis shows that the purinergic P2X7 receptor controls the release of CD14 in extracellular vesicles playing a key role in cytokine production, bacterial clearance, and survival.

Sepsis-induced numerical loss of naive autoantigen-specific CD4 T cells reduces host capacity to develop autoimmune immune disease, thereby demonstrating an intriguing relationship between infection and autoimmune disease.

Sepsis-induced long-term muscle weakness was reproduced using a refined murine model, which was accompanied by mitochondrial dysfunction in the absence of sustained atrophy, suggesting the promise of mitochondria-targeted post-sepsis therapies.