![]() In particular, we evidenced TGF-β hyperproduction in the skin of mice deprived of dietary AhR ligands, explaining Langerhans cell retention. Mechanistically, dietary AhR ligands regulated the inflammatory profile of epidermal cells, without affecting barrier function. In addition, lack of dietary AhR ligands worsened asthma-like allergy in a model of ‘atopic march.’ Mice deprived of dietary AhR ligands displayed impaired Langerhans cell migration, leading to exaggerated T cell responses. ![]() This phenomenon was tissue-specific as airway allergy was unaffected by the diet. In cutaneous papain-induced allergy, we found that lack of dietary AhR ligands exacerbates allergic responses. Here, we addressed the influence on allergic responses of dietary agonists of aryl hydrocarbon receptor (AhR). However, the mechanisms involved remain incompletely understood. Dietary compounds can affect the development of inflammatory responses at distant sites. ![]()
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