The Microbiome, Timing, and Barrier Function in the Context of Allergic Disease  Duane R. Wesemann, Cathryn R. Nagler  Immunity  Volume 44, Issue 4, Pages 728-738 (April 2016) DOI: 10.1016/j.immuni.2016.02.002 Copyright © 2016 Elsevier Inc. Terms and Conditions

Figure 1 The Barrier Regulation Hypothesis of Allergic Disease (A) In healthy individuals, both food-allergen-specific and bacteria-induced Treg cells cooperate with ILC-derived IL-22-dependent effector functions (e.g., mucus secretion, induction of AMPs) to maintain barrier integrity and mucosal homeostasis. Allergy protective bacterial populations residing in the proximal colon might secrete metabolites or influence cellular migration from that site to regulate allergen uptake in the small intestine. (B) In food allergic subjects, the loss of these allergy-protective bacterial populations impairs barrier integrity. Increased allergen contact and depletion of metabolites like SCFAs stress the epithelial layer. Both DCs and ILC2s are primed by epithelial derived cytokines to induce a Th2 cell response and CSR to IgE, both locally and in peripheral LN. Immunity 2016 44, 728-738DOI: (10.1016/j.immuni.2016.02.002) Copyright © 2016 Elsevier Inc. Terms and Conditions