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Amphiregulin-producing T2 cells facilitate esophageal fibrosis of eosinophilic esophagitis. | LitMetric

AI Article Synopsis

  • - Massive eosinophil infiltration in eosinophilic esophagitis (EoE) can lead to esophageal fibrosis, but the specific mechanisms are not fully understood.
  • - Researchers created a mouse model of EoE to study immune cell behavior and found increased T2 cells producing amphiregulin and IL-5 in fibrotic areas after exposure to house dust mites.
  • - The study showed that higher levels of amphiregulin-producing CD4 T cells correlate with greater fibrosis in EoE patients, suggesting that targeting amphiregulin could be a new therapeutic strategy.

Article Abstract

Background: Massive eosinophil infiltration into the esophagus is associated with subepithelial fibrosis and esophageal stricture in patients with eosinophilic esophagitis (EoE). However, the pathogenesis of esophageal fibrosis remains unclear.

Objective: We sought to elucidate the cellular and molecular mechanisms underlying the induction of esophageal fibrosis.

Methods: We established a murine model of EoE accompanied by fibrotic responses following long-term intranasal administration of house dust mite antigen. Using this murine model, we investigated the characteristics of immune cells infiltrating the fibrotic region of the inflamed esophagus using flow cytometry and histological analyses. We also analyzed the local inflammatory sites in the esophagus of patients with EoE using single-cell RNA sequencing, flow cytometry, and immunohistochemistry.

Results: Enhanced infiltration of both amphiregulin-producing and IL-5-producing T2 cells was detected in the fibrotic area of the esophagus in mice subjected to repeated house dust mite exposure. Deletion of amphiregulin in CD4 T cells ameliorates esophageal fibrosis. An analysis of human esophageal biopsy samples showed that the infiltration of amphiregulin-producing CD4 T cells was higher in patients with EoE than in control patients. Furthermore, the number of infiltrated amphiregulin-producing CD4 T cells was associated with the degree of esophageal fibrosis in patients with EoE.

Conclusions: Amphiregulin, produced by T2 cells, contributes to esophageal fibrosis in EoE and may be a therapeutic target.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11260569PMC
http://dx.doi.org/10.1016/j.jacig.2024.100287DOI Listing

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