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Editorial
. 2010 Dec;126(6):1205-7.
doi: 10.1016/j.jaci.2010.10.031.

TGF-β1: Mediator of a feedback loop in eosinophilic esophagitis--or should we really say mastocytic esophagitis?

J Pablo Abonia, James P Franciosi, Marc E Rothenberg
Editorial

TGF-β1: Mediator of a feedback loop in eosinophilic esophagitis--or should we really say mastocytic esophagitis?

J Pablo Abonia et al. J Allergy Clin Immunol. 2010 Dec.
No abstract available

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Figures

Figure 1
Figure 1
A proposed model to explain molecular and cellular mechanisms involved in EE pathogenesis, TGFβ1-associated pathology, eosinophil recruitment and treatments. Aeroallergen and food allergen sensitization have been implicated in EE pathogenesis. Elemental diet, glucocorticoids, and anti-IL-5 treatments have been noted to improve the microscopic features of EE acting at different levels on the disease pathogenesis. Hyperplasic epithelial cells of the esophagus overexpress eotaxin-3 likely in response to IL-13. Eotaxin-3 overexpression promotes chemoattraction of CCR3+ eosinophils. EE disease susceptibility is genetically defined by strong association to SNPs in the TSLP gene with lesser contribution of SNPs in the FLG gene. TGFβ1 and Th2 cytokines promote IL-9 generation which promotes mastocytosis. Th2 cytokines (e.g. IL-13 and IL-4) drive eotaxin-3 production, as well as synergize with TGFβ1 to promote Th9 cells which drive mastocytosis, thereby resulting in a positive feedback loop as mast cells and eosinophils produce TGFβ1. TGFβ1 has been shown to induce several processes that promote the EE disease pathogenesis including fibrosis, smooth muscle contractility, and periostin expression, which further promotes tissue remodeling and regulates eotaxin-mediated eosinophil adhesion and migration.
See this image and copyright information in PMC

Comment on

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