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Arterial Inflammation in Mice Lacking the Interleukin 1 Receptor Antagonist Gene
It is shown that mice that are homozygous for a null mutation in the gene encoding an endogenous antiinflammatory cytokine, interleukin 1 receptor antagonist (IL-1ra), develop lethal arterial inflammation involving branch points and flexures of the aorta and its primary and secondary branches, suggesting that expression of IL-1 is likely to have a significant role in signaling artery wall damage.
The new IL-1 family member IL-1F8 stimulates production of inflammatory mediators by synovial fibroblasts and articular chondrocytes
IL-1F8 exerts proinflammatory effects in primary human joint cells, and it remains to be determined whether circulating IL-1f8 can contribute to joint inflammation in rheumatoid arthritis.
A new nomenclature for IL-1-family genes.
A tissue specific IL‐1 receptor antagonist homolog from the IL‐1 cluster lacks IL‐1, IL‐1ra, IL‐18 and IL‐18 antagonist activities
IL‐1L1 had no detectable agonistic or antagonistic effect on IFN‐γ production in response to IL‐18 in KG‐1 cells and was concluded, contrary to a recent suggestion made by others, that IL‐ 1L1 is not a functional IL‐1ra.
A sequence-based map of the nine genes of the human interleukin-1 cluster.
Six novel genes encoding proteins with the interleukin (IL)-1 fold have been identified recently, allowing determination of the gene structures, precise localization of exons, and determination of distances between conventional SNP and microsatellite markers.
Airway epithelial cell differentiation during lung organogenesis requires C/EBPα and C/EBPβ
It is demonstrated that C/EBPα and C/ EBPβ play pivotal, and partly overlapping roles in determining airway epithelial differentiation, with possible implications for tissue regeneration in lung homeostasis and disease.
Lung epithelial CCAAT/enhancer-binding protein-β is necessary for the integrity of inflammatory responses to cigarette smoke.
  • L. Didon, J. Barton, M. Nord
  • Medicine, Biology
    American journal of respiratory and critical care…
  • 15 July 2011
The data suggest a previously unknown role for C/EBPβ and the airway epithelium in mediating inflammatory and innate immune responses to cigarette smoke.
The pattern recognition receptor Nod1 activates CCAAT/enhancer binding protein β signalling in lung epithelial cells
The results demonstrate a novel pathway downstream of the nucleotide-binding oligomerisation domain protein 1 receptor in these cells and suggest that C/EBPβ may play a role in immune responses to meso-diaminopimelic acid-containing bacteria in the lung.
Characterization of RNA aptamers that disrupt the RUNX1–CBFβ/DNA complex
High-affinity RNA aptamers represent new reagents that target a novel surface on the RHD required to stabilize the recombinant RHD–CBFβ complex and thus will further aid exploring the functions of this key transcription factor.