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      IgE responses to exogenous and endogenous allergens in atopic dermatitis patients under long‐term systemic cyclosporine A treatment

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          Abstract

          Atopic dermatitis ( AD) patients mount IgE antibody responses to a variety of environmental allergens and also to autoantigens. We analyzed serum samples from four AD patients who had received oral cyclosporine A (CyA) treatment for up to 17 months regarding IgE autoreactivity to nitrocellulose‐blotted human epithelial cell extracts and IgE levels to environmental allergens by quantitative ImmunoCap measurements. Skin inflammation was assessed by SCORAD. During full‐dose treatment, a strong reduction in T‐cell‐mediated skin symptoms was observed which reappeared when CyA treatment was reduced or stopped. The intensity of IgE autoreactivity seemed to follow skin inflammation as it was reduced during full‐dose treatment and increased upon inflammation. Interestingly, IgE levels to exogenous allergens were boosted by allergen exposure, declined thereafter, and seemed to be unaffected by CyA. Our data thus indicate that allergen‐specific IgE production is boosted by allergen contact and cannot be reduced by CyA‐mediated T‐cell suppression.

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          Most cited references15

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          Th2 Cytokines and Atopic Dermatitis.

          Atopic dermatitis (AD), a chronic relapsing inflammatory skin disease, is increasing in prevalence around the world. Intensive research is ongoing to understand the mechanisms involved in the development of AD and offer new treatment options for patients suffering from AD. In this review, we highlight the importance of allergic Th2 responses in the development of the disease and summarize relevant literature, including genetic studies, studies of human skin and mechanistic studies on keratinocytes and mouse models of AD. We discuss the importance of the skin barrier and review recent findings on the pro-Th2 cytokines TSLP, IL-25, and IL-33, notably their ability to polarize dendritic cells and promote Th2 responses. After a brief update on the contribution of different T-cell subsets to AD, we focus on Th2 cells and the respective contributions of each of the Th2 cytokines (IL-4, IL-13, IL-5, IL-31, and IL-10) to AD. We conclude with a brief discussion of the current gaps in our knowledge and technical limitations.
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            Molecular spreading and predictive value of preclinical IgE response to Phleum pratense in children with hay fever.

            IgE sensitization against grass pollen is a cause of seasonal allergic rhinitis. We sought to investigate the evolution at the molecular level and the preclinical predictive value of IgE responses against grass pollen. The German Multicentre Allergy Study examined a birth cohort born in 1990. A questionnaire was administered yearly, and blood samples were collected at 1, 2, 3, 5, 6, 7, 10, and 13 years of age. Grass pollen-related seasonal allergic rhinitis (SARg) was diagnosed according to nasal symptoms in June/July. Serum IgE antibodies to Phleum pratense extract and 8 P pratense molecules were tested with immune-enzymatic singleplex and multiplex assays, respectively. One hundred seventy-seven of the 820 examined children had SARg. A weak monomolecular/oligomolecular IgE response to P pratense was observed very frequently before SARg onset. These initial IgE responses increased in concentration and molecular complexity during the preclinical and clinical process. A typical progression of IgE sensitization was observed: Phl p 1 (initiator in >75% of cases); then Phl p 4 and Phl p 5; then Phl p 2, Phl p 6, and Phl p 11; and then Phl p 12 and Phl p 7. At age 3 years, IgE sensitization predicted SARg by age 12 years (positive predictive value, 68% [95% CI, 50% to 82%]; negative predictive value, 84% [95% CI, 80% to 87%]). At this preclinical prediction time, the number of recognized molecules and the serum levels of IgE to P pratense were significantly lower than at 3 or more years after SARg onset. The IgE response against grass pollen molecules can start years before disease onset as a weak monosensitization or oligosensitization phenomenon. It can increase in serum concentration and complexity through a "molecular spreading" process during preclinical and early clinical disease stages. Testing IgE sensitization at a preclinical stage facilitates prediction of seasonal allergic rhinitis at its molecular monosensitization or oligosensitization stage. Copyright © 2012 American Academy of Allergy, Asthma & Immunology. Published by Mosby, Inc. All rights reserved.
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              Early childhood IgE reactivity to pathogenesis-related class 10 proteins predicts allergic rhinitis in adolescence.

              Component-resolved diagnosis might improve the prediction of future allergy in young children.
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                Author and article information

                Journal
                Allergy
                Allergy
                10.1111/(ISSN)1398-9995
                ALL
                Allergy
                John Wiley and Sons Inc. (Hoboken )
                0105-4538
                1398-9995
                17 September 2015
                January 2016
                : 71
                : 1 ( doiID: 10.1111/all.2016.71.issue-1 )
                : 115-118
                Affiliations
                [ 1 ] Division of Immunopathology Department of Pathophysiology and Allergy ResearchCenter for Pathophysiology, Infectiology and Immunology Medical University of Vienna ViennaAustria
                [ 2 ] Department of Dermatology Allergy UnitUniversity Hospital Zürich ZürichSwitzerland
                [ 3 ]Present address: Max Planck Institute of Psychiatry MunichGermany
                Author notes
                [*] [* ] Correspondence

                Birgit Linhart, PhD, Division of Immunopathology, Department of Pathophysiology and Allergy Research, Center for Pathophysiology, Infectiology and Immunology, Medical University of Vienna, Waehringer Guertel 18‐20, 1090 Vienna, Austria

                Tel.: +43 1 40400 51150

                Fax: +43 1 40400 51300

                E‐mail: birgit.linhart@ 123456meduniwien.ac.at

                Article
                ALL12711
                10.1111/all.12711
                4950058
                26234649
                1742cc92-54f7-41c1-80a6-6d5e2bc0df29
                © 2015 The Authors. Allergy Published by John Wiley & Sons Ltd.

                This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                : 27 July 2015
                Page count
                Pages: 4
                Funding
                Funded by: Austrian Science Fund (FWF)
                Award ID: P23350‐B11
                Award ID: F4605
                Categories
                Brief Communication
                Brief Communications
                Custom metadata
                2.0
                all12711
                January 2016
                Converter:WILEY_ML3GV2_TO_NLMPMC version:4.9.2 mode:remove_FC converted:19.07.2016

                Immunology
                allergy,atopic dermatitis,cyclosporin a,ige
                Immunology
                allergy, atopic dermatitis, cyclosporin a, ige

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