Allergic diseases affect up to one third of individuals in the developed world during their lifetime, causing severe loss in the quality of life and a significant burden on healthcare services. Food allergy is a growing public health concern affecting 6-8% of children and 3-5% of adults with life-threatening potential. Environmental factors related to a modern lifestyle have been implicated in the increased prevalence of food allergy in recent years.
Food allergy can be defined as clinical immune responses to normally harmless food allergens. This disease is typically associated with CD4+ T cells that secrete pathogenic T helper (Th) 2 cytokines, and with allergen-specific immunoglobulin (Ig) E antibodies that trigger the release of inflammatory mediators from mast cells and circulating basophils. An aberrant response to food allergens can also be non-IgE-mediated. Normally, the ingestion of foods results in oral tolerance and therefore, food allergy is thought to be due to a failure of oral tolerance. Recent studies have suggested that alterations in (i) regulatory T cell functions; (ii) Th2 responses; (iii) microbiota, and/or (iv) food sensitization via alternative routes, such as the skin, are likely contribute to the failure of oral tolerance and to the development of food allergy. However, the mechanisms responsible for the breakdown in oral tolerance remain poorly understood.
There is currently no cure for food allergy, other than strict avoidance of identified foods. Key problems in this field that remain to be resolved are our (i) insufficient understanding of the mechanisms of the breakdown in oral tolerance in food allergy and (ii) our lack of understanding of the reasons why such mechanisms have recently taken such a strong basis within the human population. We are at an exciting point in time in which discoveries about the etiology, mechanisms, treatment, and prevention of food allergy are critical for guiding future areas of research and for identifying therapeutic options for food allergic patients.
In this Research Topic, we aim to provide an overview of recent progress in our understanding of food allergy. We welcome the submission of Reviews, Mini-Reviews, Original Research, and Clinical Trial articles that cover, but are not limited to, the following topics:
1. Environmental and genetic risk factors for food allergy.
2. Mechanisms of food allergy: effector immune cells involved in the initiation, development and manifestations of disease.
3. Regulatory immune mechanisms in tolerance against food allergy.
4. Prevention and treatment of food allergy.
5. Eosinophilic esophagitis and food allergy.
Allergic diseases affect up to one third of individuals in the developed world during their lifetime, causing severe loss in the quality of life and a significant burden on healthcare services. Food allergy is a growing public health concern affecting 6-8% of children and 3-5% of adults with life-threatening potential. Environmental factors related to a modern lifestyle have been implicated in the increased prevalence of food allergy in recent years.
Food allergy can be defined as clinical immune responses to normally harmless food allergens. This disease is typically associated with CD4+ T cells that secrete pathogenic T helper (Th) 2 cytokines, and with allergen-specific immunoglobulin (Ig) E antibodies that trigger the release of inflammatory mediators from mast cells and circulating basophils. An aberrant response to food allergens can also be non-IgE-mediated. Normally, the ingestion of foods results in oral tolerance and therefore, food allergy is thought to be due to a failure of oral tolerance. Recent studies have suggested that alterations in (i) regulatory T cell functions; (ii) Th2 responses; (iii) microbiota, and/or (iv) food sensitization via alternative routes, such as the skin, are likely contribute to the failure of oral tolerance and to the development of food allergy. However, the mechanisms responsible for the breakdown in oral tolerance remain poorly understood.
There is currently no cure for food allergy, other than strict avoidance of identified foods. Key problems in this field that remain to be resolved are our (i) insufficient understanding of the mechanisms of the breakdown in oral tolerance in food allergy and (ii) our lack of understanding of the reasons why such mechanisms have recently taken such a strong basis within the human population. We are at an exciting point in time in which discoveries about the etiology, mechanisms, treatment, and prevention of food allergy are critical for guiding future areas of research and for identifying therapeutic options for food allergic patients.
In this Research Topic, we aim to provide an overview of recent progress in our understanding of food allergy. We welcome the submission of Reviews, Mini-Reviews, Original Research, and Clinical Trial articles that cover, but are not limited to, the following topics:
1. Environmental and genetic risk factors for food allergy.
2. Mechanisms of food allergy: effector immune cells involved in the initiation, development and manifestations of disease.
3. Regulatory immune mechanisms in tolerance against food allergy.
4. Prevention and treatment of food allergy.
5. Eosinophilic esophagitis and food allergy.
