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IL-1Ra Gene (il-1ra + gene)

Distribution by Scientific Domains
Medical Sciences100%

Selected Abstracts

Study on VNTR polymorphism of gene IL-1RA in 19 Chinese populations

INTERNATIONAL JOURNAL OF IMMUNOGENETICS, Issue 2 2010
J. Jiang
Summary Earlier studies suggested that a variable number tandem repeat (VNTR) polymorphism in intron 2 of the interleukin-1 receptor antagonist (IL-1RA) gene might be associated with some chronic inflammatory diseases, autoimmune diseases and solid tumours. To study the distribution of this polymorphism in China, 1352 samples were collected from 19 widely distributed Chinese populations. PCR was used to genotype the VNTR. The overall frequencies of allele 1 and allele 2 were 0.913 and 0.064 respectively. The frequency of the allele 2 was significantly different between the northeastern and the northwestern populations. Moreover, the allele frequencies at this locus in three Chinese Han populations were different from that in minority populations. When compared with other populations worldwide, the frequencies of the two alleles in China were not significantly different from those in the Asian and Pacific Islands. However, the prevalence of allele 1 in China was significantly higher, and the prevalence of allele 2 was significantly lower, than those in American and European Caucasians, and the pairwise Fst values reinforced this observation. The differences of the allele frequencies between different regions and within the same region showed that geography and race have important roles in the population differentiation for the IL-1RA gene. In summary, our results provide a valuable reference for population genetic information and future disease association studies in Chinese populations. [source]

A preliminary in vitro study into the use of IL-1Ra gene therapy for the inhibition of intervertebral disc degeneration

INTERNATIONAL JOURNAL OF EXPERIMENTAL PATHOLOGY, Issue 1 2006
Christine L. Le Maitre
Summary Conventional therapies for low back pain (LBP) are purely symptomatic and do not target the cause of LBP, which in approximately 40% of cases is caused by degeneration of the intervertebral disc (DIVD). Targeting therapies to inhibit the process of degeneration would be a potentially valuable treatment for LBP. There is increasing evidence for a role for IL-1 in DIVD. A natural inhibitor of IL-1 exists, IL-1Ra, which would be an ideal molecular target for inhibiting IL-1-mediated effects involved in DIVD and LBP. In this study, the feasibility of ex vivo gene transfer of IL-1Ra to the IVD was investigated. Monolayer and alginate cultures of normal and degenerate human intervertebral disc (IVD) cells were infected with an adenoviral vector carrying the IL-1Ra gene (Ad-IL-1Ra) and protein production measured using an enzyme-linked immunosorbent assay. The ability of these infected cells to inhibit the effects of IL-1 was also investigated. In addition, normal and degenerate IVD cells infected with Ad-IL-1Ra were injected into degenerate disc tissue explants and IL-1Ra production in these discs was assessed. This demonstrated that both nucleus pulposus and annulus fibrosus cells infected with Ad-IL-1Ra produced elevated levels of IL-1Ra for prolonged time periods, and these infected cells were resistant to IL-1. When the infected cells were injected into disc explants, IL-1Ra protein expression was increased which was maintained for 2 weeks of investigation. This in vitro study has shown that the use of ex vivo gene transfer to degenerate disc tissue is a feasible therapy for the inhibition of IL-1-mediated events during disc degeneration. [source]

IL-1 receptor antagonist gene polymorphism in idiopathic recurrent spontaneous abortion in a Chinese Han population

INTERNATIONAL JOURNAL OF IMMUNOGENETICS, Issue 5 2010
M. Z. Dai
Summary Interleukin-1 receptor antagonist (IL-1Ra) has been supposed to play important roles in pregnancy. The purpose of this study was to evaluate the association between the polymorphisms of IL-1Ra gene (IL1RN) variable number tandem repeat (VNTR) in intron 2 with idiopathic recurrent spontaneous abortion (RSA). Ninety-two RSA patients and hundred normal women with at least one live birth and no history of miscarriage were included in the study. Frequencies of the IL1RN alleles and genotypes were determined. Data revealed that the prevalence of IL1RN allele and genotype was not significant between the RSA and control group (all P > 0.05). Our finding indicated that the polymorphism VNTR of IL1RN gene in intron 2 may not be a risk factor for RSA in the Chinese Han population. [source]

IL-10 modulates cytokine gene transcription by protein synthesis-independent and dependent mechanisms in lipopolysaccharide-treated neutrophils

EUROPEAN JOURNAL OF IMMUNOLOGY, Issue 11 2007
Marzia Rossato
Abstract We have recently reported that the ability of IL-10 to rapidly exert its anti-inflammatory effects on human neutrophils is dependent upon exposure of these cells to LPS for at least 3,4,h. Here, we demonstrate that, in neutrophils "preconditioned" by LPS, IL-10 primarily targets the transcription of TNF-,, CXCL8 and IL-1ra genes, as revealed by primary transcript real-time RT-PCR. We also show that IL-10-induced transcriptional repression of TNF-, and CXCL8 genes consists of two distinct phases: an early one, occurring rapidly and in a protein synthesis-independent manner, followed by a second phase, more delayed and dependent on protein synthesis. Interestingly, the protein synthesis dependence of the latter phase coincides with a reduced ability of IL-10 to induce STAT3 tyrosine phosphorylation. Importantly, inhibition of IL-10-induced STAT3 activation and IL-10-suppressive action by a prolonged exposure to cycloheximide (CHX) was observed to occur also in human monocytes and was caused by a defective IL-10-mediated activation of Jak1 and Tyk2 kinases. Taken together, our findings suggest that CHX interferes with the IL-10-mediated intracellular signaling pathway by interrupting events upstream of STAT3 activation. These data question the concept of the requirement of an IL-10-induced mediator as the unique mechanism to execute IL-10 anti-inflammatory program. [source]