1. Volume 157, Issue 1, Pages 17-20 (July 2019)
Local Antigen Deposition in Eosinophilic Esophagitis: Implications for Immune Activation 
Seema S. Aceves 
Gastroenterology 
Volume 157, Issue 1, Pages (July 2019)
DOI: /j.gastro
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2. Figure 1
Potential immune effects of esophageal antigen deposition. Inhaled and ingested allergens land on a previously disrupted esophageal epithelium in eosinophilic esophagitis (EoE) or promote epithelial barrier disruption via endogenous protease activity. The epithelial barrier in eosinophilic esophagitis loses integrity due to the loss of protease inhibitors such as serine peptidase inhibitor Kazal type 7 (SPINK7), adherens proteins such as E-cadherin, and tight junction proteins such as claudins. Loss of barrier integrity allows the penetration of aeroallergen and food antigens into the esophagus and uptake by antigen presenting cells. Local antigen presentation by dendritic cells and other antigen presenting cells promotes T helper type 2 cells (Th2) skewing in an already atopic person and the production of cytokines such as IL-5 that promotes eosinophil infiltration and IL-4 and IL-13, which cause B-cell class switching to IgE. Eosinophil-derived interleukins such as IL-9 promote mast cell accumulation and survival and further barrier disruption. Local IgG4 production may be involved in fibrosis. IgE bound to mast cells causes degranulation in the presence of antigen specific IgE with the release of preformed cytokines such as transforming growth factor-β1 and tumor necrosis factor-α, which promote myofibroblast transformation and fibroblast production of extracellular matrix proteins. Together these insults cause fibrosis, rigidity, and dysmotility.
Gastroenterology  , 17-20DOI: ( /j.gastro )
Copyright © 2019 AGA Institute Terms and Conditions