Immunoglobulin E Response to Human Proteins in Atopic Patients
Rudolf ValentaRenate SteinerSusanne SeiberlerDieter MaurerWolfgang R. SperrPeter ValentSusanne SpitzauerS. KapiotisJosef S. SmolenGeorg Stingl
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Experimental sensitization in dogs has revealed that the capacity to produce high levels of IgE against a variety of allergens (high IgE responders), an essential characteristic of the atopic state, is a genetic trait inherited in a dominant manner. In high IgE responder dogs spontaneous development of IgE to inhaled allergens, such as house dust mites, on the other hand, represents an apparent phenotype very similar to that observed in human atopic families. The full potential of the high IgE response gene appears to be fulfilled only under some conditions such as early and repeated exposition to allergens. It is therefore quite possible that the true phenotype of human atopy would also be inherited in a dominant fashion but not constantly expressed. This would explain why the increase in the prevalence of allergic diseases started long before the environmental factors currently accused could have been at play. This hypothesis, which can be verified experimentally, has important implications for the future of allergy.
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Atopy is a heterogeneous condition that differs from patient to patient. Some patients are sensitized to one allergen only whereas others are sensitized to many. The immune response appears to differ in patients sensitized to single or multiple allergens. Patients allergic to a single allergen have a significantly less intense IgE immune response, develop symptoms later in the allergy season, and respond better to standard immunotherapy than do patients who are allergic to multiple allergens. An explanation for this heterogeneity may reside in different patterns of release of cytokines that play a major role in regulating the synthesis of IgE. These include IL-4, which induces IgE synthesis, and interferon gamma, which suppresses IgE synthesis.
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Serum Dermatophagoides farinae-specific IgE RAST (DF IgE) levels were assayed in 122 atopic dermatitis patients at the first examination. From the statistical study, we found trimodality of the individual variability of serum DF IgE levels. We hypothesize that serum DF IgE levels may be controlled by a pair of allelic genes.
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Alopecia areata (AA) is often observed in patients with atopic dermatitis (AD) although the etiology is unclear. Previous studies have provided evidence that a history of atopy and/or autoimmune diseases is a risk factor for AA [1, 2]. Furthermore, the serum levels of total immunoglobulin E (IgE) were also significantly higher in AA patients than in controls [3, 4]. However, the immunopathology of AA associated with AD and/or a high serum IgE titer is still unclear. We hypothesized that the pathomechanism [...]
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The objective of this study is to evaluate if there is a difference in the occurrence of asthma bronchiale, rhinitis, pollen allergy, food allergy and sensitization to basic food allergens, onset of atopic dermatitis (AD), family history about atopy, and duration of eczematic lesions in AD patients with the level of total immunoglobulin E (IgE) under or above 200 IU/ml. Complete allergological and dermatological examination was performed and the statistical evaluation of the relations among the patients with the level of IgE under 200 IU/ml and above 200 IU/ml was performed. Out of 277 patients suffering from AD, we included 87 men and 190 women; the average age was 25.9 years. From 277 patients, 92 patients (33%) have IgE under 200 IU/ml; in these patients, the occurrence of tested parameters is significantly lower in comparison to patients with IgE above 200 IU/ml.
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Numerous studies, based upon the frequency of allergic and auto-immune disorders in association with selective deficiency in IgA, as well as the abnormally high proportion of IgA deficiency in atopic patients, have led to the hypothesis that allergy results from a deficiency in IgA during the first months of life. Thus subjects with an initial transient deficiency in IgA (followed by normal or greater than average production) produce an excess of IgE. The aim of this study, carried out by multifactorial data analysis, was to determine whether serum IgE levels were related to those of IgA. Comparison of the serum Ig levels of 4 groups of individuals, with or without IgA deficiency, showed that the production of IgE was more closely related to the respiratory condition responsible than to IgA levels. According to IgA and E levels, the 4 groups differ distinctly, atopic patients without asthma constituting a "bridge" between the control group and those with asthma. In the presence of an apparently identical situation, i.e. an IgA deficiency, individuals may react in two different ways: some produce an abundance of IgE whilst others fail to do so and are more susceptible to recurrent infective episodes. The role of the genetic control of IgE as well as environmental factors in the pathogenesis of allergic manifestations is discussed.
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Coined 80 years ago, the term 'atopy' to designate a group of diseases associated with IgE and a hereditary background has raised many discussions. In particular, it is difficult to consider as part of an atopic syndrome cases of IgE-mediated allergies to isolated allergens without evidence of a familial inheritance. The postulate expressed in this essay is that in humans we are essentially dealing with an atopic IgE-mediated allergy, which is the equivalent of a genetically determined high IgE response, and with a nonatopic IgE-mediated allergy, which is the equivalent of a low IgE response in mammals and rodents.
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Eosinophilic Esophagitis
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A 3-year-old body was evaluated for the possible diagnosis of hyperimmunoglobulin E syndrome (HIES). From the age of 4 months he developed significant atopy and was subsequently diagnosed with severe atopic dermatitis, asthma, and allergic rhinitis, with moderately high total serum IgE levels. Because IgE production has been shown to be regulated by cytokines produced by the CD4+ helper T lymphocyte subsets, we measured the circulating levels of cytokines representative of these cellular subsets in this patient. We therefore measured serum levels of interleukin-4 (IL-4), the Th2 subset-derived cytokine that upregulates IgE synthesis, as well as the levels of interferon-γ and interferon-α (IFN-γ/α), cytokines produced by the Th1 subset that inhibit IL-4-mediated IgE upregulation. We found that in this patient, IL-4 levels were normal, indicating normal Th2 activity. The levels of IFN-γ were higher than normal, but the serum IFN-α levels in this patient were undetectable and were actually below the normal range. Thus, even though both IFN-γ and IFN-α have been shown to be necessary for controlling IL-4 actions, the selective absence of IFN-α, even in the presence of normal or increased amounts of IFN-γ, could permit IL-4 induced IgE production. Lack of IFN-α may explain this patient's recurrent infections, as well as IgE-induced atopic conditions. Our data in this study with the patient showing selective deficiency of IFN-α but not of IFN-γ provide support for the role of IFN-α in the pathogenesis of atopic dermatitis. The findings in this patient clearly warrant further studies of IFN-α in patients with atopic disorders.
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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.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.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.
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