T‐cell activation genes differentially expressed at birth in CD4⁺ T‐cells from children who develop IgE food allergy

Abstract

Although transient, suboptimal neonatal T-cell activation pathways that signal through the NF-κB complex may affect the developmental transition of T-cell phenotypes in the periphery shortly after birth and may increase the risk of food allergy.

Useful biomarkers for assessing the adverse health effects of PCBs in allergic children: pediatric molecular epidemiology

“…Nevertheless, despite the wealth of information about the relationship between IL-8 and asthma, no one has investigated whether IL-8 is a useful biomarker for examining the link between PCB exposure and childhood asthma. Study 2: as IL-22 has often been demonstrated to be associated with allergic diseases [17,22,[31][32][33], it is not surprising that we found it to be associated with egg-and milk-specific IgE reactions in this study. However, none of the previous studies addressed whether IL-22 expression is associated with PCB exposure.…”

Epigenome-wide association study reveals longitudinally stable DNA methylation differences in CD4+ T cells from children with IgE-mediated food allergy

“…10,14 As part of this previous analysis, CD4+ T-cells were activated using anti-CD3 and driven through polyclonal expansion for 24 h after which time gene expression profiles were measured. In the current study, we analyzed available DNA samples from individuals at baseline (unstimulated) to examine whether pre-existing differences in DNA methylation might underscore suboptimal CD4+ T-cell gene expression.…”

“…13 We have previously demonstrated that dysregulated neonatal CD4+ T-lymphocyte responses are a feature of pediatric food allergy. 14 Using gene expression profiling, we compared the , and susan Prescott Food allergy is mediated by a combination of genetic and environmental risk factors, potentially mediated by epigenetic mechanisms. cD4+ T-cells are key drivers of the allergic response, and may therefore harbor epigenetic variation in association with the disease phenotype.…”

Genome-scale profiling reveals a subset of genes regulated by DNA methylation that program somatic T-cell phenotypes in humans

“…Raw data files were exported from Genome Studio (Illumina, San Diego, CA, USA) into the R statistical environment (http://cran.r-project.org/index.html). Data quality was assessed using the methylumi package [39][40][41] to assess signal-to-noise ratios, and identify outlying samples and batch effects. All samples passed QC.…”

“…The microarray data were preprocessed with the PLIER algorithm (gcbg background subtraction, quantile normalization, iterPLIER summarization). [41][42][43] Data were variance stabilized by adding 16 to all data points, followed by log2 transformation in the R environment (http://cran.r-project.org/).…”