Interleukin (IL)-1-like protein 1 (IL-1L1) is a 155-amino acid protein that shares 27% identity with IL-1 g and 47% with IL-1 receptor antagonist (IL-1ra). A 2.7-kb IL-1L1 mRNA was cloned from human placenta and is detectable in the trophoblastic cell line JEG-3, in macrophages and in endotoxin-stim
IL-1 receptor antagonist (IL-1Ra) plasma levels are co-ordinately regulated by both IL-1Ra and IL-1β genes
✍ Scribed by Mikko Hurme; Sari Santtila
- Publisher
- John Wiley and Sons
- Year
- 1998
- Tongue
- English
- Weight
- 59 KB
- Volume
- 28
- Category
- Article
- ISSN
- 0014-2980
No coin nor oath required. For personal study only.
📜 SIMILAR VOLUMES
## Abstract The pro‐inflammatory cytokine interleukin‐1 (IL‐1), contributes to neuronal inflammation and cell death induced by ischemia, excitotoxicity, or trauma, while administration of IL‐1 receptor antagonist (IL‐1ra) reduces neuronal injury. The aim of the present study was to test the hypothe
## Abstract ## BACKGROUND The principal components of the interleukin‐1 (IL‐1) family are two secreted factors (IL‐1α and IL‐1β), two transmembrane receptors (IL‐1RI [biologically active] and IL‐1RII [inert receptor]), and a natural antagonist receptor of IL‐1 function (IL‐1Ra). Changes in the exp
The eye is considered an immunologically privileged organ and is separated from the rest of the body by blood-ocular barriers. Part of the blood-retina barrier consists of the retinal pigment epithelium (RPE). In addition to the physical barrier which the monolayer of RPE cells forms, these cells co
Proinflammatory cytokines, including interleukin (IL)-1, are known to modulate effects of neurotoxic neurotransmitters discharged during excitation or inflammation in the central nervous system (CNS). They also regulate development of glial scars at sites of CNS injury. To elucidate a genetic predi
## Abstract The purpose of this study was to evaluate whether IL‐1 β (IL‐1β promoter and IL‐1β exon 5), IL‐1 receptor antagonist (IL‐1 __Ra__), and IL‐4 (IL‐4 promoter and IL‐4 intron 3) gene polymorphisms act as markers of susceptibility to Kawasaki disease (KD), or of the severity of the disease.