Stephen C Dreskin1, Matthew Germinaro2, Dominik Reinhold3, Xueni Chen1, Brian P Vickery4, Michael Kulis5, A Wesley Burks5, Surendra S Negi6, Werner Braun6, Jeffery M Chambliss7, Spodra Eglite1, Caitlin M G McNulty8. 1. Division of Allergy and Clinical Immunology, Departments of Medicine and Immunology, University of Colorado Denver, Aurora, CO, USA. 2. Janssen R&D US, LLC, Spring House, PA, USA. 3. PPD, Wilmington, NC, USA. 4. Department of Pediatrics, Emory University School of Medicine, Atlanta, GA, USA. 5. Division of Allergy and Immunology, Department of Pediatrics, University of North Carolina-Chapel Hill, NC, USA. 6. Sealy Center for Structural Biology and Molecular Biophysics, Department of Biochemistry and Molecular Biology, The University of Texas Medical Branch, Galveston, TX, USA. 7. Division of Allergy and Immunology, Department of Pediatrics, University of Texas, Dallas, TX, USA. 8. St. Paul Allergy and Asthma in St. Paul, MN, USA.
Abstract
BACKGROUND: For patients with peanut allergy, there are currently no methods to predict who will develop sustained unresponsiveness (SU) after oral immunotherapy (OIT). OBJECTIVE: Assess IgE binding to peanut (PN), Ara h 2, and specific linear epitopes of Ara h 2 as predictors of the important clinical parameters: eliciting dose threshold and attainment of SU following OIT. METHODS: Samples and clinical data were collected from children undergoing OIT. PN- and Ara h 2-sIgE were quantified by ImmunoCAP® . IgE binding to linear peptides of Ara h 2 and Ara h 6 was measured with peptide microarrays. RESULTS: Values of PN-sIgE correlated with eliciting dose (P = .001) and with a higher likelihood of achieving SU (P < .0001), but these relationships were lost at higher values for PN-sIgE (≥14 kIU for eliciting dose and ≥35 kIU/L for SU). In subjects with PN-sIgE ≥ 14 kIU/L, binding of IgE to epitopes 5 and 6 of Ara h 2 was associated with a lower eliciting dose at baseline challenge (P < .001; Pc < .02). In subjects with PN-sIgE ≥ 35 kIU/L, a combined model of IgE binding to epitopes 1, 5 and 6 with PN-sIgE was highly predictive of attainment of SU (AUC of 0.86; P = .0067). CONCLUSION: In young patients with peanut allergy, measurement of PN-sIgE and IgE binding to specific linear epitopes of Ara h 2 in baseline samples may allow stratification of patients regarding sensitivity to challenge and outcome of OIT.
BACKGROUND: For patients with peanutallergy, there are currently no methods to predict who will develop sustained unresponsiveness (SU) after oral immunotherapy (OIT). OBJECTIVE: Assess IgE binding to peanut (PN), Ara h 2, and specific linear epitopes of Ara h 2 as predictors of the important clinical parameters: eliciting dose threshold and attainment of SU following OIT. METHODS: Samples and clinical data were collected from children undergoing OIT. PN- and Ara h 2-sIgE were quantified by ImmunoCAP® . IgE binding to linear peptides of Ara h 2 and Ara h 6 was measured with peptide microarrays. RESULTS: Values of PN-sIgE correlated with eliciting dose (P = .001) and with a higher likelihood of achieving SU (P < .0001), but these relationships were lost at higher values for PN-sIgE (≥14 kIU for eliciting dose and ≥35 kIU/L for SU). In subjects with PN-sIgE ≥ 14 kIU/L, binding of IgE to epitopes 5 and 6 of Ara h 2 was associated with a lower eliciting dose at baseline challenge (P < .001; Pc < .02). In subjects with PN-sIgE ≥ 35 kIU/L, a combined model of IgE binding to epitopes 1, 5 and 6 with PN-sIgE was highly predictive of attainment of SU (AUC of 0.86; P = .0067). CONCLUSION: In young patients with peanutallergy, measurement of PN-sIgE and IgE binding to specific linear epitopes of Ara h 2 in baseline samples may allow stratification of patients regarding sensitivity to challenge and outcome of OIT.
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