Immunology of Food Allergy Leticia Tordesillas, M. Cecilia Berin, Hugh A. Sampson  Immunity  Volume 47, Issue 1, Pages 32-50 (July 2017) DOI: 10.1016/j.immuni.2017.07.004 Copyright © 2017 Elsevier Inc. Terms and Conditions

Figure 1 Innate Immune Mechanisms Contributing to Sensitization Factors triggering innate responses, such as damage or adjuvant activity, promote production of cytokines by epithelial cells, acting on innate immune cells such as ILC2s, DCs, and basophils. DCs upregulate OX40L, priming T cells toward a Th2 cell reponses. ILC2s and basophils are involved in an amplification loop of Th2 cell responses by producing Th2 cytokines. Th2 cells promote IgE class switching on B cells through production of IL-4. IgE on the membrane of mast cells and basophil is responsible for clinical symptoms after antigen cross-linking. IL-9 is crucial for the expansion of mast cells that contribute to food allergy symptoms. Mast cells and ILC2s contribute to the suppression of tolerance responses by production of IL-4. Immunity 2017 47, 32-50DOI: (10.1016/j.immuni.2017.07.004) Copyright © 2017 Elsevier Inc. Terms and Conditions

Figure 2 The Dual Exposure Hypothesis of Food Allergy and Tolerance Exposure to antigens through the oral route results in a tolerance response, involving CD103+ DCs that are instructed toward a tolerance phenotype promoted by local factors such as GM-CSF and Muc2. CD103+ DCs migrate to the mesenteric lymph nodes to induce Treg cells. By contrast, antigen exposure through eczematous skin (including damage or bacterial toxins) leads toward sensitization. Cytokine release by epithelial cells instructs skin DCs. DCs transport the antigen to the draining lymph nodes where Th2 and Tfh cells are generated. The two pathways (sensitization and tolerance) regulate each other through inhibitory mast cell/Treg cell interactions. Immunity 2017 47, 32-50DOI: (10.1016/j.immuni.2017.07.004) Copyright © 2017 Elsevier Inc. Terms and Conditions