Molecular and cellular mechanisms of food allergy and food tolerance

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 n...

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Bibliographic Details
Published inJournal of allergy and clinical immunology Vol. 137; no. 4; pp. 984 - 997
Main Authors Chinthrajah, R. Sharon, Hernandez, Joseph D., Boyd, Scott D., Galli, Stephen J., Nadeau, Kari C.
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 01.04.2016
Elsevier Limited
Subjects
Allergens - immunology
Allergy and Immunology
Antigens
basophils
Chemokines
Cytokines
Dendritic cells
Dermatitis, Atopic - complications
Dermatitis, Atopic - immunology
desensitization
Desensitization, Immunologic - methods
Dietary Proteins - immunology
Food
Food allergies
Food allergy
Food Hypersensitivity - etiology
Food Hypersensitivity - immunology
Food Hypersensitivity - microbiology
Food Hypersensitivity - therapy
Gastrointestinal Microbiome
Homeostasis
Human subjects
Humans
Immune Tolerance
Immunoglobulins
Immunotherapy
Inflammation
Ligands
Lymphatic system
Lymphocytes
mast cells
microbiome
Probiotics - therapeutic use
Proteins
regulatory T cells
Risk Factors
sensitization
Studies
T cell receptors
tolerance
Food allergy
SLIT
GALT
regulatory T cells
DNFB
Treg
GPR
basophils
mast cells
microbiome
SCFA
desensitization
MLN
dendritic cells
APC
EPIT
immunotherapy
M cell
sensitization
OIT
OVA
Foxp3
tolerance
DC
Gut-associated lymphoid tissue
Epicutaneous immunotherapy
2,4-Dinitrofluorobenzene
Microfold cell
Mesenteric lymph node
Forkhead box protein 3
Regulatory T
Antigen-presenting cell
Dendritic cell
Ovalbumin
Sublingual immunotherapy
Oral immunotherapy
Short-chain fatty acid
G protein–coupled receptor
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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.
AbstractList 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.
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.
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.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.
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 may 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 may in part overlap with those associated with the development of natural oral tolerance.
Author Boyd, Scott D.
Nadeau, Kari C.
Chinthrajah, R. Sharon
Hernandez, Joseph D.
Galli, Stephen J.
AuthorAffiliation b Department of Pediatrics, Stanford University School of Medicine, Stanford, CA
e Sean N. Parker Center for Allergy & Asthma Research, Stanford University School of Medicine, Stanford, CA
d Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA
a Department of Medicine, Stanford University School of Medicine, Stanford, CA
c Department of Pathology, Stanford University School of Medicine, Stanford, CA
AuthorAffiliation_xml – name: b Department of Pediatrics, Stanford University School of Medicine, Stanford, CA
– name: d Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA
– name: e Sean N. Parker Center for Allergy & Asthma Research, Stanford University School of Medicine, Stanford, CA
– name: c Department of Pathology, Stanford University School of Medicine, Stanford, CA
– name: a Department of Medicine, Stanford University School of Medicine, Stanford, CA
Author_xml – sequence: 1
  givenname: R. Sharon
  surname: Chinthrajah
  fullname: Chinthrajah, R. Sharon
  organization: Department of Medicine, Stanford University School of Medicine, Stanford, Calif
– sequence: 2
  givenname: Joseph D.
  surname: Hernandez
  fullname: Hernandez, Joseph D.
  organization: Department of Pediatrics, Stanford University School of Medicine, Stanford, Calif
– sequence: 3
  givenname: Scott D.
  surname: Boyd
  fullname: Boyd, Scott D.
  organization: Department of Pathology, Stanford University School of Medicine, Stanford, Calif
– sequence: 4
  givenname: Stephen J.
  surname: Galli
  fullname: Galli, Stephen J.
  organization: Department of Pathology, Stanford University School of Medicine, Stanford, Calif
– sequence: 5
  givenname: Kari C.
  surname: Nadeau
  fullname: Nadeau, Kari C.
  email: knadeau@stanford.edu
  organization: Department of Medicine, Stanford University School of Medicine, Stanford, Calif
BackLink https://www.ncbi.nlm.nih.gov/pubmed/27059726$$D View this record in MEDLINE/PubMed
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Issue 4
Keywords Food allergy
SLIT
GALT
regulatory T cells
DNFB
Treg
GPR
basophils
mast cells
microbiome
SCFA
desensitization
MLN
dendritic cells
APC
EPIT
immunotherapy
M cell
sensitization
OIT
OVA
Foxp3
tolerance
DC
Gut-associated lymphoid tissue
Epicutaneous immunotherapy
2,4-Dinitrofluorobenzene
Microfold cell
Mesenteric lymph node
Forkhead box protein 3
Regulatory T
Antigen-presenting cell
Dendritic cell
Ovalbumin
Sublingual immunotherapy
Oral immunotherapy
Short-chain fatty acid
G protein–coupled receptor
Language English
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Snippet Ingestion of innocuous antigens, including food proteins, normally results in local and systemic immune nonresponsiveness in a process termed oral tolerance....
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SubjectTerms Allergens - immunology
Allergy and Immunology
Antigens
basophils
Chemokines
Cytokines
Dendritic cells
Dermatitis, Atopic - complications
Dermatitis, Atopic - immunology
desensitization
Desensitization, Immunologic - methods
Dietary Proteins - immunology
Food
Food allergies
Food allergy
Food Hypersensitivity - etiology
Food Hypersensitivity - immunology
Food Hypersensitivity - microbiology
Food Hypersensitivity - therapy
Gastrointestinal Microbiome
Homeostasis
Human subjects
Humans
Immune Tolerance
Immunoglobulins
Immunotherapy
Inflammation
Ligands
Lymphatic system
Lymphocytes
mast cells
microbiome
Probiotics - therapeutic use
Proteins
regulatory T cells
Risk Factors
sensitization
Studies
T cell receptors
tolerance
Title Molecular and cellular mechanisms of food allergy and food tolerance
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https://dx.doi.org/10.1016/j.jaci.2016.02.004
https://www.ncbi.nlm.nih.gov/pubmed/27059726
https://www.proquest.com/docview/1780705278
https://www.proquest.com/docview/1779883864
https://www.proquest.com/docview/1785235484
https://pubmed.ncbi.nlm.nih.gov/PMC5030841
Volume 137
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