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Search Results: 1 - 10 of 1001 matches for " interleukin-13 "
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Clinical Investigation of the Role of Interleukin-4 and Interleukin-13 in the Evolution of Prostate Cancer
Robert Goldstein,Charles Hanley,Jonathan Morris,Declan Cahill,Ashish Chandra,Peter Harper,Simon Chowdhury,John Maher,Sophie Burbridge
Cancers , 2011, DOI: 10.3390/cancers3044281
Abstract: Prostate cancer is the most common cancer in men, both in the USA and Europe. Although incurable, metastatic disease can often be controlled for years with anti-androgen therapy. Once the disease becomes castrate resistant, the median survival is 18 months. There is growing evidence that the immune system, and in particular cytokines, play an important role in prostate cancer immunosurveillance and progression. Here, we have undertaken a clinical investigation of the role of two closely related cytokines, IL-4 and IL-13 in prostate cancer. In the largest series studied to date, we show that serum IL-4, but not IL-13 is significantly elevated in castrate resistant, compared to androgen sensitive disease. Notably however, serum IL-4 levels are also raised in patients with benign prostatic disease. Analysis of benign and malignant prostate tissue demonstrates that the source of IL-4 is epithelial cells rather than infiltrating leukocytes. Together, our data are consistent with a dual role for IL-4 in prostate cancer development. In benign disease, our data add to the evidence that IL-4 serves a protective role. By contrast, the data support a direct role for IL-4 in the progression of prostate cancer from androgen responsive, to advanced castrate-resistant disease.
Interleukin-4 receptor alpha gene variants and allergic disease
Ian P Hall
Respiratory Research , 2000, DOI: 10.1186/rr3
Abstract: Several genome-wide screens have now been performed in different populations, looking for susceptibility genes for asthma and allergic disease. In general, the results of these genome screens have been somewhat disappointing in that, although chromosomal regions showing linkage have been identified, the strength of linkage at any given site has been inconsistent. These data suggest that a number of genes of moderate effect rather than a small number of genes with marked effects contribute to the genetic basis of allergic disease.To try to dissect out the important candidate genes that contribute to the risk of developing asthma or its important sub-phenotypes, several groups have concentrated on strong candidate genes that map to known susceptibility loci for asthma and atopy. Several such candidates have been identified (Table 1), including the gene for interleukin-4 receptor α (IL-4Rα), which is situated on chromosome 16p and is known to contain a number of polymorphisms. The recent paper from Carole Ober and colleagues [1] provides important information on the potential relevance of IL-4Rα gene variants in determining the risk of developing atopic disease.The IL-4Rα subunit forms part of the signalling complex for IL-4 itself but also serves as the α chain of the IL-13 receptor. Both IL-4 and IL-13 themselves have been implicated as potential candidate genes in the development of asthma, both being present in the TH2 cytokine locus on chromosome 5q23-31 [2]. Both IL-4 and IL-13 have overlapping functions, including mediating isotype switching to IgE synthesis.Several previous studies have suggested association and/or linkage between IL-4Rα gene variants and allergic disease, although not all studies have been positive. Mitsuyasu et al [3] reported the Ile50 allele of the IL-4Rα to be associated with atopic asthma, whereas Kruse et al [4] reported an association between the Pro478 and Arg551 alleles and low IgE levels. Hershey et al [5] reported an association bet
The gene encoding interleukin-13: a susceptibility locus for asthma and related traits
Marsha Wills-Karp
Respiratory Research , 2000, DOI: 10.1186/rr7
Abstract: Asthma is a complex inflammatory lung disease controlled by both environmental and genetic factors. Although the exact genes controlling susceptibility to asthma have not been identified, several genome-wide searches have provided evidence for the linkage of asthma or asthma-related traits (serum IgE levels, skin test reactivity, bronchial hyper-responsiveness, blood eosinophils) to loci on multiple autosomal chromosomes [1,2,3,4,5,6]. Of particular interest is the 5q31-33 region, which contains the T helper type 2 (Th2) cytokine gene cluster [interleukin (IL)-4, IL-13, IL-5 and IL-9] and has been linked to asthma or related phenotypes in many studies [2,3,4,5,6,7,8]. In addition to the linkage data, many human and animal studies have implicated these cytokines, either individually or in concert, in the pathophysiology of asthma. Of the Th2 cytokines in this chromosomal region, IL-4 has been extensively studied because it is known to be important in the differentiation of T cells into Th2 cytokine-producing cells. A polymorphism has been identified in the promoter of this gene (-590C/T) [9] which was initially associated with elevated serum IgE levels. This polymorphism has been associated with asthma in some studies [10,11] but not in others [12,13,14]. Thus attention has turned to other genes in this region. Recent studies in animal models that support the dominance of the gene encoding IL-13, which resembles IL-4, in the allergic response have spurred an extensive study of this molecule in susceptibility to asthma [15,16,17].The gene encoding IL-13 is located only 25 kilobases upstream of the gene for IL-4 and in the same orientation, leading to the speculation that these genes arose as a duplication event during evolution. In addition to their structural similarities they share considerable functional similarities. They are both known to have a number of actions relevant to the asthmatic diathesis such as the regulation of isotype class switching in B cells to I
Cytokine profile associated with human chronic schistosomiasis mansoni
Magalh?es, Andréa;Miranda, Delfin Gonzalez;Miranda, Roberval Gonzalez;Araújo, Maria Ilma;Jesus, Adriana Almeida de;Silva, Angela;Santana, Luciana B;Pearce, Edward;Carvalho, Edgar M;Jesus, Amélia Ribeiro de;
Memórias do Instituto Oswaldo Cruz , 2004, DOI: 10.1590/S0074-02762004000900004
Abstract: this study objective was to evaluate the cytokines associated with early events of hepatic fibrosis in schistosomiasis mansoni. hepatic fibrosis was classified by ultrasonography in 94 patients. immunological evaluation was performed by measurement of secreted cytokines (interleukin il-5, il-10, il-13, interferon-g, tumor necrosis factor-a and transforming growth factors-b) in peripherl blood mononuclear cells stimulated by schistosoma mansoni antigens. significantly, higher levels of il-5, il-10 and il-13 were found in supernatants of sea-stimulated pbmc from subjects with degree iii hepatic fibrosis as compared to patients with degree i or ii fibrosis, significant increases in il-5 and il-13 levels were also observed in some of the subjects who remained untreated for one year following initial assessment and developed more serious fibrosis during this period. the data suggests a role for type 2 cytokines in early stages of hepatic fibrosis in human schistosomiasis mansoni.
In vitro initial immune response against Leishmania amazonensis infection is characterized by an increased production of IL-10 and IL-13
Coêlho, Zirlane Castelo B;Teixeira, Maria Jania;Mota, Erika Freitas;Frutuoso, Mércia Sindeaux;Silva, Jo?o Santana da;Barral, Aldina;Barral-Netto, Manoel;Pompeu, Margarida Maria L;
Brazilian Journal of Infectious Diseases , 2010, DOI: 10.1590/S1413-86702010000500009
Abstract: the initial encounter of leishmania with its host's immune system is important in the outcome of infection. previous studies have shown that pbmcs from healthy volunteers (hv) exposed to leishmania differ in ifn-γ production. we have expanded such observations evaluating the profile and kinetics of cytokines (ifn-γ, il-12p70, il-10, il-13), chemokines (ccl5, ccl3, ccl4, cxcl10), and chemokine receptors (ccr1,ccr5, cxcr3, ccr4) in vitro l. amazonensis-stimulated of hv's pbmcs. hvs were divided in groups of high (hr) or low (lr) ifn-γ responders. in both groups, hr and lr, after l. amazonensis infection there was a predominance of il-10 and il-13 over ifn-γ production, while il-12 was produced in similar amount. regarding chemokines, a more striking difference was observed for ccl3 expression that was lower at 12 hours and 48 hours post infection in lr than in hr. interestingly, a downregulation of ccr5 and a greater expression of ccr4 were found in low ifn-γ responders. these data suggest that early after l. amazonensis infection there is a cytokine milieu dominated by il-13 and il-10, and despite of this environment, ifn-γ is produced, supporting the complexity of the response. it is noteworthy that the pattern of immune response is mounted in first hours after leishmania stimulation, with the definition of the differentiation of th1 versus th2 cells. it remains to be determined if such an in vitro difference has an in vivo counterpart in terms of susceptibility to infection
Avalia??o das citocinas IL-10 e IL-13 como mediadores na progress?o da fibrose de Symmers em portadores de esquistossomose mans?nica na forma hepatoesplênica
Brandt, Carlos Teixeira;Rino, Mario;Pitta, Maira Galdino da Rocha;Muniz, Janinne Siqueira;Silveira, Diego de Oliveira;Castro, Célia Maria Machado Barbosa de;
Revista do Colégio Brasileiro de Cirurgi?es , 2010, DOI: 10.1590/S0100-69912010000500005
Abstract: objective: to investigate the serum levels of il-10 and il-13 in patients with hepatosplenic schistosomiasis mansoni (hsm), evaluating the role of these cytokines in the development of hepatic fibrosis. methods: the study was prospective and analytical, developed at the department of surgery, federal university of pernambuco, keizo asami laboratory of immunology. we studied three groups: group i - 25 patients with hepatosplenic schistosomiasis mansoni who were not submitted to surgery; group ii - 30 individuals who underwent splenectomy and ligature of left gastric vein; group iii - 33 subjects without hepatosplenic schistosomiasis mansoni or any other disease or condition that could compromise the hepatic functional reserve. serum concentrations of il-10 and il-13 were obtained through elisa. considering their non-parametric nature, all concentrations were analyzed by kruskal-wallis test, with p<0.05 used to reject the null hypothesis. results: the mean concentrations of il-10 in ng/ml in serum were gi: 50.0 ± 59.0; gii: 38.0 ± 270; giii: 38.0 ± 20.0. concentrations of il-13 in ng/ml in the serum of patients were respectively: 41.0 ± 93.0 in gi, 16.0 ± 17.0 in gii and 18.0 ± 34.0 in giii. there was no significant difference between the mean concentrations of il-10 and il-13 between the study groups (p> 0.05). conclusion: the mean serum concentrations of il-10 and il-13 were similar in all three groups, indicating that possibly the presence of these cytokines in serum is not associated with different degrees of symmers fibrosis in patients with hepatosplenic schistosomiasis mansoni.
Local IL-13 gene transfer prior to immune-complex arthritis inhibits chondrocyte death and matrix-metalloproteinase-mediated cartilage matrix degradation despite enhanced joint inflammation
Karin CAM Nabbe, Peter LEM van Lent, Astrid EM Holthuysen, Annet W Slo?tjes, Alisa E Koch, Timothy RDJ Radstake, Wim B van den Berg
Arthritis Research & Therapy , 2005, DOI: 10.1186/ar1502
Abstract: One of the main pathological features of rheumatoid arthritis is marked destruction of cartilage [1]. This destruction starts with reversible proteoglycan depletion, which is followed by irreversible cartilage degradation defined as chondrocyte death and breakdown of collagen type II, eventually leading to matrix erosion. The latter is mainly induced by matrix metalloproteinases (MMPs), which generate specific cleavage sites within matrix molecules [2,3]. MMPs are secreted in an inactive form by IL-1-stimulated chondrocytes, synovial macrophages, and fibroblasts [4-6]. Activation of MMPs is still poorly understood, but MMP activity is primarily found in experimental immune-complex (IC)-dependent arthritis models.Immunoglobulin G (IgG)-containing ICs can activate macrophages upon recognition by Fcγ receptors (FcγRs). Three classes of murine FcγR can be distinguished: FcγRI, II, and III. Triggering FcγRI and III activates cellular responses, whereas FcγRII is an inhibitory receptor [7]. Previous studies have showed that activating FcγRI and III are crucial in induction of severe cartilage destruction, since chondrocyte death and MMP-mediated cartilage damage were absent in FcγR-deficient mice after induction of immune-complex-mediated arthritis (ICA) [8]. Furthermore, cartilage damage is aggravated by local overexpression of the proinflammatory T helper (Th)1 cytokine IFNγ [9]. This increase in cartilage destruction was observed only in IC-dependent arthritis models [9]. FcγRI was found to be crucial in the induction of chondrocyte death, whereas both FcγRI and III mediated MMP-mediated expression of VDIPEN [9].Since the Th1 cytokine IFNγ worsens the arthritic response by up-regulation of the activating FcγRs, overexpression of a Th2 cytokine during arthritis might be protective, because of down-regulation of these receptors. In earlier studies, we found that adenoviral overexpression of IL-4 resulted in reduced MMP-mediated cartilage damage and chondrocyte death duri
Lebrikizumab in the personalized management of asthma
Thomson NC, Patel M, Smith AD
Biologics: Targets and Therapy , 2012, DOI: http://dx.doi.org/10.2147/BTT.S28666
Abstract: rikizumab in the personalized management of asthma Review (3067) Total Article Views Authors: Thomson NC, Patel M, Smith AD Published Date September 2012 Volume 2012:6 Pages 329 - 335 DOI: http://dx.doi.org/10.2147/BTT.S28666 Received: 01 July 2012 Accepted: 07 August 2012 Published: 14 September 2012 Neil C Thomson,1 Manish Patel,2 Andrew D Smith2 1Institute of Infection, Immunity, and Inflammation, University of Glasgow and Respiratory Medicine, Gartnavel General Hospital, Glasgow, UK; 2Department of Respiratory Medicine, Wishaw Hospital, Wishaw, Lanarkshire, UK Abstract: There is a need for improved therapies for severe asthma. Lebrikizumab, a humanized monoclonal antibody that binds to interleukin (IL)-13, is under development for the treatment of poorly controlled asthma. This article reviews the potential role of IL-13 in the pathogenesis of asthma, the efficacy and safety of lebrikizumab in humans, and progress in patient selection for lebrikizumab therapy. IL-13 is a T-helper (Th2) cell-derived cytokine implicated in inflammatory responses in asthma, including serum immunoglobulin-E synthesis, mucus hypersecretion, and subepithelial fibrosis. Blocking the pro-inflammatory effects of IL-13 with lebrikizumab has the potential to improve asthma control. Published data on the efficacy and safety of lebrikizumab in the treatment of asthma are relatively limited. The late asthmatic response after inhaled allergen challenge is reduced by almost 50%, following treatment with lebrikizumab. In a Phase II study performed in 219 adults with poorly controlled asthma despite inhaled corticosteroids (MILLY trial), lebrikizumab produced an improvement in prebronchodilator forced expiratory volume in 1 second of 5.5% compared with placebo at 12 weeks, but had no effects on other efficacy end points. Adverse effects were similar to placebo, except that musculoskeletal side effects occurred slightly more often with lebrikizumab. Stratifying patients into a high Th2 phenotype using serum periostin, which is upregulated in lung epithelial cells by IL-13, may identify individuals responsive to blockade of IL-13. In the MILLY trial, lebrikizumab treatment was associated with greater improvement in lung function in patients with elevated serum periostin levels compared with those with low periostin levels. Two large Phase III randomized controlled trials in patients with uncontrolled asthma are underway to establish the safety and efficacy of lebrikizumab when administered over a 52-week period. These studies will also help to determine whether identifying patients with a Th2 high inflammatory phenotype using serum periostin allows a personalized approach to the treatment of asthma.
Serum levels of interleukin (IL)-13, IL-17 and IL-18 in patients with ischemic heart disease
Abdollah Jafarzadeh,Ali Esmaeeli-Nadimi,Hossain Nough,Maryam Nemati
Anadolu Kardiyoloji Dergisi , 2009,
Abstract: Objective: It has been reported that the cytokines play an important role in the pathogenesis of cardiovascular diseases. The aim of this study was to evaluate the serum levels of interleukin (IL)-13, IL-17 and IL-18 in patients with ischemic heart disease (IHD) and also to clarify their association with traditional risk factors of disease.Methods: A total of 60 patients with IHD as having acute myocardial infarction (AMI; n=30) or unstable angina (UA; n=30) and 30 sex- and age- matched healthy subjects as a control group were enrolled to this cross-sectional, case-controlled study. Serum samples were collected from all participants (for AMI patients at 3-5 days after events and for UA at admission time) and tested for the IL-13, IL-17 and IL-18 by use of ELISA method. Statistical analysis was performed using ANOVA, Student t, Kruskal-Wallis, Mann-Whitney U and Chi-square tests as appropriate. Results: The frequencies of subjects with detectable levels of IL-13 were 6.7%, 20% and 33.3% in AMI, UA and control groups, respectively. The frequency of subjects with detectable levels of IL-13 in control group was significantly higher as compared to AMI group and total group of patients with IHD (p<0.02 and p<0.05, respectively). The mean serum levels of IL-17 in AMI group (6.68±1.2 pg/ml) and UA group (5.48±1.01 pg/ml) were significantly higher than that observed in control group (2.07±0.60 pg/ml; p<0.005 and p<0.04, respectively). Moreover, the mean serum levels of IL-18 in UA group (122.92±18.16 pg/ml) were significantly higher than in control group (67.82±5.98 pg/ml; p<0.03). The mean serum levels of IL-18 in IHD patients without a certain traditional risk factor including non-hypertensive patients (120.14±17.04 pg/ml), non-dyslipidemic patients (131.86±20.04 pg/ml), non-diabetic patients (111.96±14.71 pg/ml) and non-smoker patients (113.93±16.41 pg/ml) were significantly higher as compared to control group (p<0.04, p<0.004, p<0.03 and p<0.03, respectively). Although, the mean serum levels of IL-18 in patients with a certain traditional risk factor were higher in comparison to control group, but the differences were not significant. The means serum levels of IL-17 in patients with or without a certain traditional risk factor were also markedly higher as compared to healthy group. Conclusions: These results showed that the higher serum levels of IL-17 and IL-18 were associated with IHD. The presence or absence of a certain traditional risk factors of IHD may influence the serum levels of cytokines. These findings may be considered to improve the predictive
Association Between the Polymorphisms of IL-4 Gene Promoter (-590C>T), IL-13 Coding Region (R130Q) and IL-16 Gene Promoter (-295T>C) and Allergic Asthma
Sara Hosseini-Farahabadi,Jalil Tavakkol-Afshari,Houshang Rafatpanah,Reza Farid-Hosseini
Iranian Journal Of Allergy, Asthma and Immunology , 2007,
Abstract: Allergic asthma is a multifactorial disease, influenced by genetic and environmental factors. Recent family-based studies have revealed evidence for linkage of human chromosomes 5q31-33, 12q15-24, 11q13 and 15q23.6 as regions likely to contain genes related to asthma. Among the candidate genes in these regions are the genes encoding for human interleukin-4, interleukin-13 and interleukin-16. To evaluate this linkage, we examined an Iranian population of patients with asthma. A total of 30 patients with allergic asthma and 50 normal subjects were studied. Allergic asthma was confirmed using skin prick test and spirometry. DNA was extracted from blood cells and IL-4 (-590C>T), IL-13 (R130Q) and IL-16 (-295T>C) polymorphisms were determined by PCR-RFLP method. Out of 30 patients with allergic asthma, the following genotypes for IL-4, IL-13 and IL-16 cytokines were found: IL-4 genotypes consisted of 17 (56.7%) CC, 8 (26.7%) CT and 5 (16.7%) TT; IL-13 genotypes consisted of 11 (36.7%) GG, 13 (43.3%) GA and 6 (20%) AA; IL-16 genotypes consisted of 23 (76.7%) TT and 7 (23.3%) CT. No patient showed CC genotype for IL-16. A higher proportion of case subjects with the C allele for the IL-4, G allele for the IL-13 and T allele for the IL-16 polymorphisms was found compared with the T, A and C alleles, respectively. These results suggest an influence of genetic variability at the promoter of IL-4 gene (-590C>T) and a coding region of IL-13 gene (R130Q) on the occurrence of allergic asthma and no relationship between IL-16 promoter polymorphism (-295T>C) and this disease.
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