Food allergy is defined as an adverse reaction to food proteins caused by immunologic mechanisms and is now estimated to affect over 12 million Americans. A 2008 CDC report indicated an 18% rise in childhood food allergy from 1997-2007 with an estimated 3.9% of children currently affected. Milk or egg allergies in infants/young children are most common (~2.5%), and typically resolve, although recent reports indicate increasing persistence beyond age 5 years. Peanut allergy now affects approximately 1% of young children, which is double the prevalence reported just over a decade ago. Peanut allergy is often severe, sometimes fatal and, in contrast to milk and egg allergy, resolves in only 20% of patients. There is only a limited understanding of the mechanisms involved in the developmental course of food allergies. For peanut allergy in particular, it is not known why only certain atopic individuals acquire this allergy, or what mechanisms are responsible for its permanence. To effectively prevent or reverse the progression of food allergy, immune interventions will be needed. Furthermore, it is likely that successful strategies will need to be directed to those persons at identifiable risk (e.g., who have biomarkers associated with development of peanut allergy). This multi-center, longitudinal observational study completed enrollment in March 2008. The cohort includes 512 infants initially age 3-15 months with likely egg/milk allergy or moderate-severe atopic dermatitis and a positive allergy prick skin test to egg or milk, but without current known peanut allergy. These criteria were employed to establish a cohort with an increased risk to have or develop peanut allergy. There has been a 98% retention rate for ongoing serial allergy assessments. Clinical information and DNA samples were also obtained from 250 of their siblings as a control group. Continuation of this study is required to determine the clinical course of peanut, egg and milk allergies. These final clinical outcomes will be used to delineate, compare and contrast biologic markers and immunologic changes associated with development of peanut allergy and loss of egg and milk allergy, while simultaneously addressing genetic and environmental influences. This cohort will also serve as a comparator group for children with eosinophilic esophagitis and for those undergoing immunotherapies to peanut as described in additional projects in this Consortium. The observational study will address hypotheses associated with 2 specific aims: 1) To evaluate immune (T cell, humoral, innate immunity) and genetic parameters (Toll-like receptor polymorphisms, filaggrin gene mutations, and others) associated with the occurrence of peanut allergy and clinical outcomes for milk/egg allergy, and 2) To evaluate environmental (diet, hygiene-related) and clinical (atopic dermatitis) factors that may influence occurrence of peanut allergy and clinical outcomes for milk/egg allergy.

Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
Research Program--Cooperative Agreements (U19)
Project #
2U19AI066738-06
Application #
8022453
Study Section
Special Emphasis Panel (ZAI1-WFD-I (M3))
Project Start
2010-07-01
Project End
2015-06-30
Budget Start
2010-07-01
Budget End
2011-06-30
Support Year
6
Fiscal Year
2010
Total Cost
$862,445
Indirect Cost
Name
Icahn School of Medicine at Mount Sinai
Department
Type
DUNS #
078861598
City
New York
State
NY
Country
United States
Zip Code
10029
Sampson, Hugh A; Berin, M Cecilia; Plaut, Marshall et al. (2018) The Consortium for Food Allergy Research (CoFAR) The First Generation. J Allergy Clin Immunol :
Chiang, David; Chen, Xintong; Jones, Stacie M et al. (2018) Single-cell profiling of peanut-responsive T cells in patients with peanut allergy reveals heterogeneous effector TH2 subsets. J Allergy Clin Immunol 141:2107-2120
Martin, Lisa J; He, Hua; Collins, Margaret H et al. (2018) Eosinophilic esophagitis (EoE) genetic susceptibility is mediated by synergistic interactions between EoE-specific and general atopic disease loci. J Allergy Clin Immunol 141:1690-1698
Berin, M Cecilia; Grishin, Alexander; Masilamani, Madhan et al. (2018) Egg-specific IgE and basophil activation but not egg-specific T-cell counts correlate with phenotypes of clinical egg allergy. J Allergy Clin Immunol 142:149-158.e8
Chehade, Mirna; Jones, Stacie M; Pesek, Robbie D et al. (2018) Phenotypic Characterization of Eosinophilic Esophagitis in a Large Multicenter Patient Population from the Consortium for Food Allergy Research. J Allergy Clin Immunol Pract 6:1534-1544.e5
Watson, C T; Cohain, A T; Griffin, R S et al. (2017) Integrative transcriptomic analysis reveals key drivers of acute peanut allergic reactions. Nat Commun 8:1943
Rochman, Mark; Travers, Jared; Miracle, Cora E et al. (2017) Profound loss of esophageal tissue differentiation in patients with eosinophilic esophagitis. J Allergy Clin Immunol 140:738-749.e3
Agashe, Charuta; Chiang, David; Grishin, Alexander et al. (2017) Impact of granulocyte contamination on PBMC integrity of shipped blood samples: Implications for multi-center studies monitoring regulatory T cells. J Immunol Methods 449:23-27
Schoos, Ann-Marie M; Kattan, Jacob D; Gimenez, Gustavo et al. (2016) Sensitization phenotypes based on protein groups and associations to allergic diseases in children. J Allergy Clin Immunol 137:1277-1280
Davis, Benjamin P; Epstein, Tolly; Kottyan, Leah et al. (2016) Association of eosinophilic esophagitis and hypertrophic cardiomyopathy. J Allergy Clin Immunol 137:934-6.e5

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