Autoimmunity and Atopic Dermatitis

Irene Mittermann; Karl J. Aichberger; Robert Bünder; Nadine Mothes; Harald Renz; Rudolf Valenta


Curr Opin Allergy Clin Immunol. 2004;4(5) 

In This Article

Abstract and Introduction

Purpose of Review: It has been demonstrated that a considerable percentage of patients suffering from atopic dermatitis mount IgE autoantibodies against a broad variety of human proteins. This review summarizes evidence for autoimmune mechanisms in atopic dermatitis and suggests novel pathomechanisms that may be involved in this disease.
Recent Findings: It has been shown that patients suffering from atopic dermatitis exhibit IgE autoreactivity to human proteins. These autoantigens are expressed in a variety of cell and tissue types. Complementary DNAs coding for IgE autoantigens have been identified, cloned and characterized at the molecular level. Using purified recombinant IgE autoantigens, it has been shown in paradigmatic models that IgE autoimmunity may be a pathogenetic mechanism in atopic dermatitis. Moreover, it has been shown that the levels of IgE autoantibodies are associated with severity of disease.
Summary: Patients suffering from severe manifestations of atopy mount IgE autoantibodies against a variety of human proteins. The levels of IgE autoantibodies correspond with disease severity. Several mechanisms of IgE autoimmunity may contribute to the pathogenesis of atopic dermatitis.

Atopic dermatitis is a chronic relapsing pruritic skin disease, which affects up to 5% of the adult population and up to 10% of children. It often progresses to asthma and allergic rhinitis later in life.[1] Atopic dermatitis is characterized by two phases: an initial phase with acute lesions, predominated by T helper cell type 2 (Th2) cytokines followed by a second Th1-dominated phase that is associated with eczematous chronic atopic dermatitis lesions. In this regard, atopic dermatitis is different from other forms of acute allergic manifestations, as it exhibits a mixture of type I and type IV-like hypersensitivity reactions. The Th1 response is associated with the predominance of interferon-γ and IL-12, whereas the Th2 immune response is associated with the predominance of IL-4, IL-5 and IL-13.[2]

Patients with atopic dermatitis often have elevated serum IgE levels and sensitization against a variety of environmental allergens, but there is also evidence that exacerbation of the disease occurs in the absence of exposure to environmental allergens.[3]

The discovery of similarities between exogenous allergens and human proteins and the demonstration of IgE autoreactivity led to the reinvestigation of the earlier described observation that certain allergic patients mount IgE reactivity against human proteins. After the discovery of profilin as an IgE-defined autoantigen,[4] other groups searched for IgE cross-reactivity between exogenous and endogenous antigens.[5,6,7] At the same time it was shown that a high percentage of patients suffering from atopic dermatitis display IgE autoreactivity to a broad spectrum of human proteins, which are expressed in a variety of cell and tissue types.[8] In contrast, atopic persons suffering from mild forms of allergy such as allergic rhinoconjunctivitis as well as healthy individuals failed to display IgE autoreactivity.[8] Moreover it has been demonstrated that the levels of IgE autoantibodies corresponded with severity of chronic atopic disease.[9,10] So far, it has been impossible to identify major IgE-defined autoantigens because patients suffering from severe forms of atopy display IgE autoreactivity against a broad variety of autoantigens. Nevertheless, several IgE autoantigens have been identified by complementary DNA cloning and were expressed as recombinant autoantigens Table 1 ).[9] The timeline in Fig. 1 summarizes the observations regarding autoimmunity in atopy.

Evidence for autoimmunity in atopic dermatitis.


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