FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W4242580373> ?p ?o ?g. }

• W4242580373 endingPage "1098" @default.
• W4242580373 startingPage "1097" @default.
• W4242580373 abstract "IgE is a central mediator of allergic disease, and therapies directed against IgE can alleviate hay fever and allergic asthma. To identify novel therapeutic targets or pathways underlying IgE regulation, Liang et al (Nature 2015; http://dx.doi.org/10.1038/nature14125) surveyed epigenetic associations between serum IgE concentrations and methylation at loci concentrated in CpG islands genome wide by using DNA from peripheral blood leukocytes. The authors confirmed that methylation at these loci differed significantly in isolated eosinophils from subjects with and without asthma and high IgE levels. Furthermore, the top 3 loci accounted for 13% of IgE variation in the primary subject panel. These results identify novel therapeutic targets and biomarkers for patient stratification for allergic diseases.Methylation at these loci differed significantly in isolated eosinophils Methylation at these loci differed significantly in isolated eosinophils We asked authors Dr William O. C. M. Cookson and Professor Miriam Moffatt from the National Heart & Lung Institute to comment on the significance of these results: “Our results indicate a primary role for eosinophils in the regulation of high IgE levels, and we conjecture that the differentially methylated loci (DMRs) represent eosinophil activation. Interleukin 5 receptor alpha (IL5RA) is one of the top hits, and may be used to identify patients most likely to respond to anti-IL-5 antibodies (such as mepolizumab and reslizumab) or antibodies directed at the IL-5 receptor (such as benralizumab). Another top hit, LPCAT2, modifies the production of PAF (a potent pro-inflammatory lipid mediator) and is likely to be an effective target for novel therapies.” Asthma is known to be exacerbated by house dust mites (HDMs), which act in vivo on the bronchial epithelial layer, and severe asthma has been associated with bronchial remodeling and, more specifically, increased bronchial smooth muscle mass. However, the relationship between HDM stimulation of the bronchial epithelial layer and bronchial smooth muscle remodeling has not been explored. Using human tissue samples, Trian et al (Am J Respir Crit Care Med 2015;191:538-46) discovered that epithelial stimulation by HDM selectively increased the proliferation of bronchial smooth muscle cells from asthmatic patients but not that of cells from nonasthmatic subjects. Moreover, the mechanism involved epithelial protease-activated receptor 2–dependent production of leukotriene C4, which was associated with overexpression of the leukotriene receptor CysLTR1 by bronchial smooth muscle cells from asthmatic patients in vitro and ex vivo. This work demonstrates the selective role of HDMs on bronchial smooth muscle remodeling in patients with severe asthma and points out different therapeutic targets.House dust mite selectively increased the proliferation of bronchial smooth muscle cells from asthmatic patients but not that of cells from nonasthmatic subjects House dust mite selectively increased the proliferation of bronchial smooth muscle cells from asthmatic patients but not that of cells from nonasthmatic subjects We asked author Patrick Berger, MD, PhD, from the Cardio-thoracic Research Centre of Bordeaux to comment on the significance of these results: “The present study demonstrates for the very first time that an orally administrated pharmacologic compound (ie, gallopamil) significantly decreases the BSM thickness in a placebo-controlled, double-blind, 12-month trial performed in patients with severe asthma.” The induction of the TH2 cell response requires antigen-presenting cells, especially dendritic cells, but the mechanisms of induction have not been fully defined. Lee et al (Proc Natl Acad Sci U S A 2015;112:1529-34) demonstrate that low cyclic AMP levels in dendritic cells induce TH2-biased responses in vitro and in vivo, whereas increasing cyclic AMP levels inhibit these responses. The authors show that mice with conditional deletion of Gnas, a gene that encodes for the heterotrimeric GTP-binding protein Gαs, which stimulates the synthesis of cyclic AMP, in dendritic cells that are atopic develop gradual TH2 and spontaneous bronchial asthma in vivo that shares multiple immunologic, biochemical, clinical, and genetic similarities with human asthma. These KO dendritic cells also induce a TH2 bias in vitro. These data suggest that regulators of cyclic AMP levels in dendritic cells, such as G protein–coupled receptors, are non–pattern recognition receptors that play a significant role in CD4 T-cell differentiation and also can play a role in the suppression of this immune/allergic response.Spontaneous bronchial asthma that shares multiple similarities with human asthma Spontaneous bronchial asthma that shares multiple similarities with human asthma The prevalence of peanut allergy among children in Western countries has doubled in the past 10 years, and peanut allergy is becoming apparent in Africa and Asia. However, in countries where peanut consumption is common during infancy, the rate of peanut allergy is extremely low. This led to the conception of the Learning Early about Peanut Allergy (LEAP) trial, which sought to determine whether early introduction of dietary peanut could serve as an effective primary and secondary strategy for the prevention of peanut allergy. Toit et al (N Engl J Med 2015;372:803-13) reported the primary findings of the trial, which included 640 infants with severe eczema, egg allergy, or both who consumed or avoided peanuts until 60 months of age. The findings showed that early and sustained consumption of peanut products was associated with a substantial and significant decrease in development of peanut allergy in high-risk infants. Conversely, peanut avoidance was associated with a greater frequency of clinical peanut allergy than was peanut consumption, which calls into question the usefulness of deliberate avoidance of peanuts as a strategy to prevent allergy. The findings of this study provide us with a new strategy to prevent peanut allergy and pave the way for further studies to see whether this prevention strategy is applicable to other foods.A substantial and significant decrease in the development of peanut allergy in high-risk infantsNews items were written by medical writer Kristina Bielewicz, MS.Find more News Beyond Our Pages online at www.jaci-nbop.blogspot.com. A substantial and significant decrease in the development of peanut allergy in high-risk infants News items were written by medical writer Kristina Bielewicz, MS. Find more News Beyond Our Pages online at www.jaci-nbop.blogspot.com." @default.
• W4242580373 created "2022-05-12" @default.
• W4242580373 creator A5056639915 @default.
• W4242580373 creator A5075387555 @default.
• W4242580373 date "2015-05-01" @default.
• W4242580373 modified "2023-09-27" @default.
• W4242580373 title "News Beyond Our Pages" @default.
• W4242580373 doi "https://doi.org/10.1016/j.jaci.2015.03.017" @default.
• W4242580373 hasPublicationYear "2015" @default.
• W4242580373 type Work @default.
• W4242580373 citedByCount "0" @default.
• W4242580373 crossrefType "journal-article" @default.
• W4242580373 hasAuthorship W4242580373A5056639915 @default.
• W4242580373 hasAuthorship W4242580373A5075387555 @default.
• W4242580373 hasBestOaLocation W42425803731 @default.
• W4242580373 hasConcept C104317684 @default.
• W4242580373 hasConcept C140173407 @default.
• W4242580373 hasConcept C141105273 @default.
• W4242580373 hasConcept C150194340 @default.
• W4242580373 hasConcept C154253233 @default.
• W4242580373 hasConcept C159654299 @default.
• W4242580373 hasConcept C190727270 @default.
• W4242580373 hasConcept C203014093 @default.
• W4242580373 hasConcept C2776042228 @default.
• W4242580373 hasConcept C2777037409 @default.
• W4242580373 hasConcept C2777832160 @default.
• W4242580373 hasConcept C2777917907 @default.
• W4242580373 hasConcept C2779185760 @default.
• W4242580373 hasConcept C33288867 @default.
• W4242580373 hasConcept C41091548 @default.
• W4242580373 hasConcept C54355233 @default.
• W4242580373 hasConcept C86803240 @default.
• W4242580373 hasConceptScore W4242580373C104317684 @default.
• W4242580373 hasConceptScore W4242580373C140173407 @default.
• W4242580373 hasConceptScore W4242580373C141105273 @default.
• W4242580373 hasConceptScore W4242580373C150194340 @default.
• W4242580373 hasConceptScore W4242580373C154253233 @default.
• W4242580373 hasConceptScore W4242580373C159654299 @default.
• W4242580373 hasConceptScore W4242580373C190727270 @default.
• W4242580373 hasConceptScore W4242580373C203014093 @default.
• W4242580373 hasConceptScore W4242580373C2776042228 @default.
• W4242580373 hasConceptScore W4242580373C2777037409 @default.
• W4242580373 hasConceptScore W4242580373C2777832160 @default.
• W4242580373 hasConceptScore W4242580373C2777917907 @default.
• W4242580373 hasConceptScore W4242580373C2779185760 @default.
• W4242580373 hasConceptScore W4242580373C33288867 @default.
• W4242580373 hasConceptScore W4242580373C41091548 @default.
• W4242580373 hasConceptScore W4242580373C54355233 @default.
• W4242580373 hasConceptScore W4242580373C86803240 @default.
• W4242580373 hasIssue "5" @default.
• W4242580373 hasLocation W42425803731 @default.
• W4242580373 hasOpenAccess W4242580373 @default.
• W4242580373 hasPrimaryLocation W42425803731 @default.
• W4242580373 hasRelatedWork W2011988545 @default.
• W4242580373 hasRelatedWork W2296881971 @default.
• W4242580373 hasRelatedWork W2477521417 @default.
• W4242580373 hasRelatedWork W2570149195 @default.
• W4242580373 hasRelatedWork W2778862808 @default.
• W4242580373 hasRelatedWork W2963862309 @default.
• W4242580373 hasRelatedWork W3013947686 @default.
• W4242580373 hasRelatedWork W3171749255 @default.
• W4242580373 hasRelatedWork W3185161420 @default.
• W4242580373 hasRelatedWork W3216356557 @default.
• W4242580373 hasVolume "135" @default.
• W4242580373 isParatext "false" @default.
• W4242580373 isRetracted "false" @default.
• W4242580373 workType "article" @default.