Cellular immunological and biochemical analyses reveal how decoy IL-1RII is induced by human CD4⁺ T cells upon TCR-stimulation and regulates the Th17-Treg balance by modulating IL-1β responsiveness in IL-1RI⁺ cells.

Sarcoidosis, a granulomatous disease characterized by macrophage and T-cell activation, is found to be associated with increased HIF-1α transcriptional activity, and modulation of HIF-1α regulates inflammatory immune responses.

IL-1β release from macrophages might be responsible for the unexplained cone segment loss in retinal degenerative diseases that are associated with subretinal inflammation, such as retinitis pigmentosa or geographic atrophy.

Reconstitution of interleukin-1β secretion in non-macrophage cells implicates how this pro-inflammatory cytokine enters into the unconventional pathway of secretion through autophagy.

A neutrophil-CAF-tumor cell IL-1β/IL-6/STAT-3 signaling axis in the pancreatic tumor microenvironment underlies the association between neutrophil-to-lymphocyte ratio dynamics and pathologic response in patients with pancreatic ductal adenocarcinoma undergoing neoadjuvant therapy.

Inflammatory bowel disease risk-gene, INAVA and the ARF-GEF ARNO, regulates non-canonical cortical actin assembly and IL-1b signaling to maintain epithelial homeostasis.

The deubiquitinating enzyme YOD1 binds to the E3 ligase TRAF6 to counteract p62/sequestosome1 mediated pro-inflammatory NF-κB signaling in response to interleukin-1.

A signal for inflammatory cell death is induced by the disruption of cellular metabolism.

CFTR modulators have potent innate anti-inflammatory properties that can be measured in clinic, both ex vivo and in vitro, which can be used to predict treatment efficacy.

AXL enables the priming of the antiviral adaptive immune response by limiting the production of type I interferons in dendritic cells.