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The Journal of Allergy and Clinical Immunology
Volume 124, Issue 2
, Pages
292-300.e97
, August 2009
Clinical efficacy and immune regulation with peanut oral immunotherapy
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Effect of peanut OIT on basophil activation. Top row, Subjects who received peanut OIT. Bottom row, Subjects in an observational study of peanut allergy. At a peanut concentration of 10 μg/mL, OIT res
Effect of peanut OIT on basophil activation. Top row, Subjects who received peanut OIT. Bottom row, Subjects in an observational study of peanut allergy. At a peanut concentration of 10 μg/mL, OIT results in significant initial changes in basophil responsiveness (∗P < .001).
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Serum levels of peanut-specific immunoglobulins during peanut OIT. In the serum of 28 subjects undergoing immunotherapy, peanut-specific IgE (A), IgG (B), and IgG4 (C) were measured by using the ImmunSerum levels of peanut-specific immunoglobulins during peanut OIT. In the serum of 28 subjects undergoing immunotherapy, peanut-specific IgE (A), IgG (B), and IgG4 (C) were measured by using the ImmunoCAP instrument. Values are log-transformed, and median and mean values are represented by black and yellow horizontal lines, respectively. A mixed model, repeated-measures ANOVA was used to determine the statistical significance between baseline and treatment time points (∗P < .0005).
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Peanut OIT leads to FAB inhibition. Blue lines represent individual data points, red line the mean. Statistical differences between pre-OIT and 12-month–post-OIT serum were determined by Wilcoxon signPeanut OIT leads to FAB inhibition. Blue lines represent individual data points, red line the mean. Statistical differences between pre-OIT and 12-month–post-OIT serum were determined by Wilcoxon signed-rank test (∗P < .001).
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Cytokines secreted from PBMCs after ConA stimulation. The plotted 6 cytokines/chemokines all had statistically significant changes versus medium alone (P < .05). Black lines are median values; red linCytokines secreted from PBMCs after ConA stimulation. The plotted 6 cytokines/chemokines all had statistically significant changes versus medium alone (P < .05). Black lines are median values; red lines are means.
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Cytokines secreted from PBMCs stimulated with crude peanut extract. The plotted 6 cytokines/chemokines all had statistically significant changes versus medium alone (P < .05). Black lines are median vCytokines secreted from PBMCs stimulated with crude peanut extract. The plotted 6 cytokines/chemokines all had statistically significant changes versus medium alone (P < .05). Black lines are median values; yellow lines are means.
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Changes of FoxP3+ Treg cells during peanut oral immunotherapy. PBMCs from 10 subjects were cultured in presence of peanut proteins, Ara h 2, or medium alone (RPMI). Paired t tests were used to determiChanges of FoxP3+ Treg cells during peanut oral immunotherapy. PBMCs from 10 subjects were cultured in presence of peanut proteins, Ara h 2, or medium alone (RPMI). Paired t tests were used to determine statistical differences between baseline and later time points (P < .05, 6 months; P < .01, 12 months).
Supported by the Food Allergy and Anaphylaxis Network, the Gerber Foundation, National Institutes of Health grant 1R01-AI068074-01A1, the Arkansas Biosciences Institute, the Dorothy and Frank Robins Family, the Food Allergy Project, and Clinical and Translational Science Award 5M01-R000030-45.
Disclosure of potential conflict of interest: A. W. Burks is a consultant for ActoGeniX NV, Intelliject, McNeil Nutritionals, and Novartis; is a minority stockholder of Allertein Therapeutics and MastCell Pharmaceuticals, Inc; is on the advisory board for The Dannon Company, Inc.; is on the expert panel for Nutricia; has received research support from the National Institutes of Health, the Food Allergy and Anaphylaxis Network, and the Wallace Research Foundation; has served as an expert witness regarding food allergy; is on the Medical Board of Directors for the Food Allergy and Anaphylaxis Network; is on the Dermatological Allergy Committee for American College of Allergy, Asthma & Immunology; is a study section member of the National Institutes of Health Hypersensitivity, Autoimmunity, and Immunodeficiency; and is on the Journal of Allergy and Clinical Immunology review board. S. M. Jones is a consultant and board member for the Food Allergy and Anaphylaxis Network and has received research support from the National Institutes of Health, the Food Allergy and Anaphylaxis Network, the National Peanut Board, Mead Johnson, and Dyax Corp. J. L. Roberts has received research support from the National Institutes of Health. A. M. Scurlock has received research support from the National Institutes of Health/National Institute of Allergy and Infectious Diseases and Genocea Biosciences. T. T. Perry has received research support from the National Institutes of Health/National Institute of Allergy and Infectious Diseases, the Robert Wood Johnson Foundation, and Arkansas Biosciences Institute, Lyon. M. Kulis has received research support from the Food Allergy Initiative. W. G. Shreffler has received research support from the Food Allergy and Anaphylaxis Network. S. Durham has provided consultancy and lectures for and has received research support from GlaxoSmithKline and ALK-Abelló. B. P. Vickery has received research support from the National Institutes of Health and Ception Therapeutics. X. Zhong has received research support from the National Institutes of Health, the American Cancer Society, and the American Heart Association. The rest of the authors have declared that they have no conflict of interest.
PII: S0091-6749(09)00813-6
doi: 10.1016/j.jaci.2009.05.022
© 2009 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.
« Previous
Next »
The Journal of Allergy and Clinical Immunology
Volume 124, Issue 2
, Pages
292-300.e97
, August 2009
