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Local Antigen Deposition in Eosinophilic Esophagitis: Implications for Immune Activation.

The mechanisms of immune activation in eosinophilic esophagitis (EoE) continue to be delineated and triggering antigens can be challenging to pinpoint. Whether antigen drives esophageal eosinophil accumulation from the outside in via the lumen, from the inside out via systemic immune signals, or both, remains enigmatic. In this issue of Gastroenterology, a study led by David Katzka and colleagues 1 at the Mayo Clinic reports the penetration of dust mite antigen into the esophageal epithelium of adults with EoE. Patients with EoE (79%) but none of the controls had detectable epithelial staining for Dermatophagoides farinae protein. This group previously reported local gluten accumulation in the EoE esophagus. 2 The observation of topical antigen deposition has intriguing implications. First, it speaks to the potential for an outside-in local immune activation. Second, it suggests that local antigen presence might be a surrogate marker for lost esophageal barrier function. Third, it is possible that the presence or absence of esophageal antigen could gauge adherence to prescribed regimens, such as gluten avoidance. EoE is a delayed T helper type 2 cell (Th2)-mediated hypersensitivity involving both innate and adaptive immune responses to what should be benign antigens. Environmental adjuvants or the intrinsic of aeroallergens, as house dust mite and cockroach, can break down epithelial barriers and unleash a protective immune cascade. House dust mite has abundant protease activity including cysteine and trypsin-, chymotryptsin-, and collagenolytic-like serine proteases. 3 There is clinical and murine model that mite can drive EoE. of serine epithelial barrier dysfunction and eosinophil infiltration, it immunologically plausible that local antigen exposure could be integral to EoE instigation and/or exacerbation. Epithelial breakdown allow local presentation by cells as dendritic cells and macrophages. the underlying concurrent atopic diatheses in patients with EoE, in this study, the immune system is already primed for a Th2-dominant response. In the face of epithelial insult, innate immune cells such as group 2 innate lymphocytes are chemoattracted, activated by thymic stromal-derived lymphopoietin and IL-33, and can