[Eosinophilic inflammation in allergic diseases]

Tissular eosinophilia is a common feature of IgE-dependent allergic diseases. The classical concept links activated Th2 lymphocytes to eosinophil attraction and activation. However, comparisons of allergic diseases with non atopic "mirror "diseases reveal more complex underlying pathophysiological mechanisms. This article explores the links between allergic asthma and intrinsic asthma or asthma of the Churg-Strauss syndrome, nasal polyposis, vernal conjunctivitis, eosinophilic esophagitis (food allergy-induced or non allergic), DRESS, Ofuji disease, and eosinophilic cystitis. The results of recent mechanistic studies show that Th2 activation coupled with tissular eosinophilia can no longer be considered a hallmark of atopy. Allergic inflammation may depend on Th1 activation (vernal conjunctivitis, DRESS, eosinophilic esophagitis, etc) and simultaneous viral infection, eliciting drug hypersensitivity (DRESS). A predominant role of the epithelium in eosinophil attraction is an alternative concept with a sound basis in eosinophilic esophagitis. This concept could lead to new therapeutics aimed at controlling epithelial eotaxin 3 expression.