TY - JOUR
T1 - Food allergy
AU - Renz, Harald
AU - Allen, Katrina J.
AU - Sicherer, Scott H.
AU - Sampson, Hugh A.
AU - Lack, Gideon
AU - Beyer, Kirsten
AU - Oettgen, Hans C.
N1 - Funding Information:
H.R. is supported by the Deutsche Zentrum fur Lungenforschung (DZL; Germany; no. 82DZL00502) and the Deutsche Forschungsgemeinschaft (DFG; Germany)-funded SFB 1021. S.H.S. is supported by grants to his institution from the Food Allergy Research and Education organization and the US National Institute of Allergy and Infectious Diseases. H.A.S. has received funding paid to his institution for grant support from the US National Institute of Allergy and Infectious Diseases. K.B. has received grant money for research from the European Union, the German Research Foundation, the German Federal Ministry for Education and Research, the Food Allergy and Anaphylaxis Network and the Foundation for the Treatment of Peanut Allergy. H.C.O. received support from US NIH grant 1R01AI119918-01, the Bunning Family Foundation, the Nanji Family Fund, the Rao Chakravorti Family Fund and the Christine Olsen and Robert Small Food Allergy Research Fund at Boston Children's Hospital. The authors thank I. Schmidt (Philipps University Marburg) for her excellent editorial assistance
Funding Information:
S.H.S. has received funding paid to his institution for grant support from HAL Allergy and has received royalties from UpToDate. H.A.S. is a part‑time employee of DBV Tech‑ nologies, serving as its chief scientific officer; he has consulted for Allertein, Hycor and UCB and he owns stock options in DBV Technologies. K.B. has received grant money for research from Aimmune, Danone, DBV, DST Diagnostic, Hipp, Hycor and ThermoFisher; she has received speaker fees or honoraria for advisory boards from Aimmune, ALK, Allergo‑ Pharma, Bausch & Lomb, Danone, HAL Allergy, Meda Pharma, MedUpdate, Nestlé, Novartis and Unilever. The remaining authors declare no competing interests.
Funding Information:
H.R. is supported by the Deutsche Zentrum für Lungen‑ forschung (DZL; Germany; no. 82DZL00502) and the Deutsche Forschungsgemeinschaft (DFG; Germany)‑funded SFB 1021.S.H.S. is supported by grants to his institution from the Food Allergy Research & Education organization and the US National Institute of Allergy and Infectious Diseases. H.A.S. has received funding paid to his institution for grant support from the US National Institute of Allergy and Infectious Diseases. K.B. has received grant money for research from the European Union, the German Research Foundation, the German Federal Ministry for Education and Research, the Food Allergy & Anaphylaxis Network and the Foundation for the Treatment of Peanut Allergy. H.C.O. received support from US NIH grant 1R01AI119918‑01, the Bunning Family Foundation, the Nanji Family Fund, the Rao Chakravorti Family Fund and the Christine Olsen and Robert Small Food Allergy Research Fund at Boston Children’s Hospital. The authors thank I. Schmidt (Philipps University Marburg) for her excellent editorial assistance.
Publisher Copyright:
© 2018 Macmillan Publishers Limited, part of Springer Nature. All rights reserved.
PY - 2018/1/4
Y1 - 2018/1/4
N2 - Food allergies manifest in a variety of clinical conditions within the gastrointestinal tract, skin and lungs, with the most dramatic and sometimes fatal manifestation being anaphylactic shock. Major progress has been made in basic, translational and clinical research, leading to a better understanding of the underlying immunological mechanisms that lead to the breakdown of clinical and immunological tolerance against food antigens, which can result in either immunoglobulin E (IgE)-mediated reactions or non-IgE-mediated reactions. Lifestyle factors, dietary habits and maternal-neonatal interactions play a pivotal part in triggering the onset of food allergies, including qualitative and quantitative composition of the microbiota. These factors seem to have the greatest influence early in life, an observation that has led to the generation of hypotheses to explain the food allergy epidemic, including the dual-allergen exposure hypothesis. These hypotheses have fuelled research in preventive strategies that seek to establish desensitization to allergens and/or tolerance to allergens in affected individuals. Allergen-nonspecific therapeutic strategies have also been investigated in a number of clinical trials, which will eventually improve the treatment options for patients with food allergy.
AB - Food allergies manifest in a variety of clinical conditions within the gastrointestinal tract, skin and lungs, with the most dramatic and sometimes fatal manifestation being anaphylactic shock. Major progress has been made in basic, translational and clinical research, leading to a better understanding of the underlying immunological mechanisms that lead to the breakdown of clinical and immunological tolerance against food antigens, which can result in either immunoglobulin E (IgE)-mediated reactions or non-IgE-mediated reactions. Lifestyle factors, dietary habits and maternal-neonatal interactions play a pivotal part in triggering the onset of food allergies, including qualitative and quantitative composition of the microbiota. These factors seem to have the greatest influence early in life, an observation that has led to the generation of hypotheses to explain the food allergy epidemic, including the dual-allergen exposure hypothesis. These hypotheses have fuelled research in preventive strategies that seek to establish desensitization to allergens and/or tolerance to allergens in affected individuals. Allergen-nonspecific therapeutic strategies have also been investigated in a number of clinical trials, which will eventually improve the treatment options for patients with food allergy.
UR - http://www.scopus.com/inward/record.url?scp=85040246808&partnerID=8YFLogxK
U2 - 10.1038/nrdp.2017.98
DO - 10.1038/nrdp.2017.98
M3 - Article
C2 - 29300005
AN - SCOPUS:85040246808
SN - 2056-676X
VL - 4
JO - Nature Reviews Disease Primers
JF - Nature Reviews Disease Primers
M1 - 17098
ER -