Allergic mechanisms of Eosinophilic oesophagitis

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• 作者：John Leung ; MD ; ^{jleung3@tuftsmedicalcenter.org" class="auth_mail" title="E-mail the corresponding author} (Consulting Physician) ; Koen Robert Beukema ; BA ^{koenbeukema@gmail.com" class="auth_mail" title="E-mail the corresponding author} (Research Intern) ; Alice Hangzhou Shen ; BA ^{ashen@tuftsmedicalcenter.org" class="auth_mail" title="E-mail the corresponding author} (Research Coordinator)
• 关键词：Eosinophilic oesophagitis ; Allergic mechanism ; Antigen sensitization ; Oral tolerance ; Pathogenesis ; t-helper lymphocyte type 2 immunity ; Food allergy ; Barrier dysfunction
• 刊名：Best Practice & Research Clinical Gastroenterology
• 出版年：2015
• 出版时间：October 2015
• 年：2015
• 卷：29
• 期：5
• 页码：709-720
• 全文大小：627 K

文摘

Eosinophilic oesophagitis (EoE) is characterized by oesophageal dysfunction and oesophageal eosinophilia refractory to proton-pump-inhibitor treatment. EoE is a food allergy, as elimination of food trigger(s) abrogates the disease, while trigger reintroduction causes recurrence. The allergic mechanism of EoE involves both IgE and non-IgE processes. There is a break in oral tolerance, the immune mechanism allowing enteric exposure to food and micro-organisms without causing deleterious immune responses. Changes in life-style, alterations in gut flora and use of antibiotics may be increasing disease prevalence. Mouse models of EoE and human studies revealed the role of regulatory T-cells and iNKT-cells in the pathogenesis. Th2-cytokines like IL-4, IL-5 and IL-13, and other cytokines like TGFβ and TSLP are involved, but perhaps no one cytokine is critically important for driving the disease. Control of EoE may require a pharmaceutical approach that blocks more than one target in the Th2-inflammatory pathway.