2010•PubMedRequires access

[Eosinophilic inflammation in allergic diseases].

D.A. Moneret‐Vautrin

Open publisher page 0 citations

Abstract

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.

About this research paper

What this paper is about

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.

Why it matters

A significance statement is not available in the OpenAlex record.

Key contribution

A contribution statement is not available in the OpenAlex record.

Method / approach

Method details are not available in the OpenAlex metadata.

Main findings

Findings are not separately available in the OpenAlex metadata.

Limitations

Limitations are not available in the OpenAlex metadata.

Applications

Application details are not available in the OpenAlex metadata.

Available abstract

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.

Key concepts: Eosinophilic esophagitis, Eosinophilia, Immunology, Eosinophil, Medicine, Atopy, Allergy, Eotaxin

Related papers

Back to paper searchBrowse research topicsOriginal source
[Eosinophilic inflammation in allergic diseases]. — Research Paper | ScholarLens