Leptomeningeal inflammation in a mouse model of multiple sclerosis triggers deeply penetrating gene changes in underlying brain tissue, described using spatial transcriptomics.

Notch signaling alters TLR-induced inflammation by skewing monocyte cell fate toward patrolling monocyte differentiation at the expense of macrophage cell fate.

A major consequence of ductal-to-squamous lineage transition in pancreatic cancer cells is to augment inflammation, which may explain the exceptionally poor clinical outcomes of squamous-subtype tumors.

During aging, the pancreatic endocrine islets undergo chronic inflammation, which is associated with a reduced capacity for self-renewal of the insulin-producing beta-cells in zebrafish.

Hyperphosphatemia, by itself and in the context of chronic kidney disease, contributes to iron restrictive anemia by directly targeting the liver and elevating proinflammatory cytokines and hepcidin, which contributes to widespread tissue injury, such as skeletal muscle wasting.

Bacteria release ATP as part of their attack in sepsis.

PEGylated PDZ peptide reduces LPS-induced systemic inflammation, restores tissue integrity, decreases pro-inflammatory cytokines, and modulates macrophage populations, showing potential as a therapeutic for systemic inflammation.

Editors' Summary: This Replication Study has reproduced some parts of the original paper but it also contains results that are not consistent with other parts of the original paper.

Impaired lysosomal acidification results in retention of iron inside lysosomes, triggering functional iron deficiency, dysfunctional mitochondria (especially mtDNA loss), and inflammation in vivo in a mouse model of lysosomal disease.

PTPN22 function is regulated by reactive oxygen species, and redox regulation of PTPN22 impacts T-cell-dependent autoimmune inflammation.