Summary of allergen-specific IgE reactivities in the AD patients.

<p>Summary of allergen-specific IgE reactivities in the AD patients.</p

Frequencies of allergen-specific IgE reactivities in the AD and SE patients as tested by MeDALL allergen chip, Immunoblotting, ImmunoCAP^™ and RAST-based dot-blot assay.

<p>Frequencies of allergen-specific IgE reactivities in the AD and SE patients as tested by MeDALL allergen chip, Immunoblotting, ImmunoCAP^™ and RAST-based dot-blot assay.</p

Demographic and clinical characterization of AD patients and controls.

<p>Demographic and clinical characterization of AD patients and controls.</p

Pie charts showing the contribution of (A), allergen sources and (B), individual allergen components to IgE sensitization.

<p>Each chart represents 100% of IgE reactivities detected in plasma from all AD patients of the respective group, severe AD (left chart) and moderate AD (right chart), in (<b>A)</b> to six allergen sources using the MeDALL allergen-chip (ISU ≥ 0.3) and to extracts of <i>M</i>. <i>sympodialis</i>, <i>S</i>. <i>aureus</i> and the human cell line A431 using immunoblotting, and in (<b>B)</b> to 25 allergen molecules using the MeDALL allergen-chip (ISU ≥ 0.3). The sizes of the segments represent the proportion of the respective in (<b>A)</b>, allergen source and in (<b>B)</b>, allergen molecule among all recognized. Allergen sources/molecules start a 12 o’clock of the pie chart and continue clock-wise as listed with the color code.</p

Genetic variants associated with the strength of the IgE response in Colombian and Swedish populations

<p>Genetic variants associated with the strength of the IgE response in Colombian and Swedish populations</p

Distribution of variants in the genes analyzed by targeted resequencing (CGA cohort)

<p>Distribution of variants in the genes analyzed by targeted resequencing (CGA cohort)</p

Descriptive of individuals selected for targeted re-sequencing from the Candidate Genes for Asthma (CGA) cohort

<p>Descriptive of individuals selected for targeted re-sequencing from the Candidate Genes for Asthma (CGA) cohort</p

The culprit insect but not severity of allergic reactions to bee and wasp venom can be determined by molecular diagnosis

<div><p>Background</p><p>Allergy to bee and wasp venom can lead to life-threatening systemic reactions. The identification of the culprit species is important for allergen-specific immunotherapy.</p><p>Objectives</p><p>To determine a panel of recombinant bee and wasp allergens which is suitable for the identification of bee or wasp as culprit allergen sources and to search for molecular surrogates of clinical severity of sting reactions.</p><p>Methods</p><p>Sera from eighty-seven patients with a detailed documentation of their severity of sting reaction (Mueller grade) and who had been subjected to titrated skin testing with bee and wasp venom were analyzed for bee and wasp-specific IgE levels by ImmunoCAP^TM. IgE-reactivity testing was performed using a comprehensive panel of recombinant bee and wasp venom allergens (rApi m 1, 2, 3, 4, 5 and 10; rVes v 1 and 5) by ISAC chip technology, ImmunoCAP and ELISA. IgG₄ antibodies to rApi m 1 and rVes v 5 were determined by ELISA and IgE/IgG₄ ratios were calculated. Results from skin testing, IgE serology and IgE/IgG₄ ratios were compared with severity of sting reactions.</p><p>Results</p><p>The panel of rApi m 1, rApi m 10, rVes v 1 and rVes v 5 allowed identification of the culprit venom in all but two of the 87 patients with good agreement to skin testing. Severities of sting reactions were not associated with results obtained by skin testing, venom-specific IgE levels or molecular diagnosis. Severe sting reactions were observed in patients showing < 1 ISU and < 2kU_A/L of IgE to Api m 1 and/or Ves v 5.</p><p>Conclusion</p><p>We identified a minimal panel of recombinant bee and wasp allergens for molecular diagnosis which may permit identification of bee and/or wasp as culprit insect in venom-sensitized subjects. The severity of sting reactions was not associated with parameters obtained by molecular diagnosis.</p></div

Genetic loci associated with the risk of having high IgE response (≥75^th percentile) to ABA-1 and <i>Ascaris</i> extract in the CGA dataset.

<p>A) Effects of the tagSNP <i>CHIA</i> rs10494133 on the risk of high IgE response to ABA-1 (filled circle) and to the <i>Ascaris</i> extract (filled square) under dominant model. B) Effects of <i>STAT6</i> rs73118440 on the risk of high IgE response to ABA-1. OR: Odds ratio; CI: confidence interval.</p

Genetic loci associated with the risk of having high IgE response to both Ascaris and common allergens.

<p>A) Effects of <i>CHI3L1</i> rs4950928 on the risk of high IgE response to ABA-1 (filled circle) and to the pollen allergen Bet v 1 (white triangle). The association with ABA-1 was detected in the CGA cohort and the association with Bet v 1 in the Swedish Eczema Cohort. <b>B)</b> Effect of <i>ABDH13</i> rs3783118 on the risk of high IgE response (≥75^th percentile) to the extracts of <i>Ascaris</i> and HDM in the CGA dataset. Risk of IgE response to the <i>Ascaris</i> extract (filled square); Risk of IgE response to the <i>D</i>. <i>pteronyssinus</i> extract (filled triangle). OR: Odds ratio; CI: confidence interval.</p