Molecular and cellular mechanisms of food allergy and food tolerance - 06/04/16
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Abstract |
Ingestion of innocuous antigens, including food proteins, normally results in local and systemic immune nonresponsiveness in a process termed oral tolerance. Oral tolerance to food proteins is likely to be intimately linked to mechanisms that are responsible for gastrointestinal tolerance to large numbers of commensal microbes. Here we review our current understanding of the immune mechanisms responsible for oral tolerance and how perturbations in these mechanisms might promote the loss of oral tolerance and development of food allergies. Roles for the commensal microbiome in promoting oral tolerance and the association of intestinal dysbiosis with food allergy are discussed. Growing evidence supports cutaneous sensitization to food antigens as one possible mechanism leading to the failure to develop or loss of oral tolerance. A goal of immunotherapy for food allergies is to induce sustained desensitization or even true long-term oral tolerance to food allergens through mechanisms that might in part overlap with those associated with the development of natural oral tolerance.
Le texte complet de cet article est disponible en PDF.Key words : Food allergy, microbiome, sensitization, desensitization, immunotherapy, tolerance, regulatory T cells, basophils, mast cells, dendritic cells
Abbreviations used : APC, DC, DNFB, EPIT, Foxp3, GALT, GPR, M cell, MLN, OIT, OVA, SCFA, SLIT, Treg
Plan
Series editors: Joshua A. Boyce, MD, Fred Finkelman, MD, and William T. Shearer, MD, PhD |
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Supported by the Sean N. Parker Center for Allergy and Asthma Research; National Institutes of Health grants R01 AR067145 (to S.J.G.) and U19AI10420901 (to S.J.G., K.C.N., S.D.B., and R.S.C.); the American Academy of Allergy, Asthma & Immunology Mylan Anaphylaxis Award and Child Health Research Institute/Lucile Packard Foundation for Children's Health awards (to J.D.H.); Stanford CTSA (UL1 TR001085); and the Department of Pathology, Stanford University. |
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Disclosure of potential conflict of interest: R. S. Chinthrajah has received a grant from the National Institutes of Health (NIH) and has had studies sponsored by DBV and Aimmune. J. D. Hernandez has received consultancy fees from LEK Consulting and has received grants from the American Academy of Allergy, Asthma & Immunology and the NIH. S. J. Galli has received grants from the NIH and Stanford University. The rest of the authors declare that they have no relevant conflicts of interest. |
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Terms in boldface and italics are defined in the glossary on page 985. |
Vol 137 - N° 4
P. 984-997 - avril 2016 Retour au numéroBienvenue sur EM-consulte, la référence des professionnels de santé.
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