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Autoimmunity (or Not) in Atopic Dermatitis

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Journal Front Immunol
Date 2019 Sep 26
PMID 31552053
Citations 17
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Abstract

Atopic dermatitis (AD), one of the most frequent inflammatory skin diseases worldwide, is believed to result from a disturbed skin barrier as well as aberrant immune reactions against harmless allergens. Starting mostly during childhood with a chronic, remitting relapsing course, the disease can persist into adulthood in about one fifth of patients. Immune reactions to self-proteins have been observed in AD patients already in the beginning of the Twentieth century, when human cellular extracts were shown to provoke skin lesions. However, the term "autoimmunity" has never been claimed, since AD is first and foremost an atopic disease. In contrast, this IgE-hallmarked autoreactivity was termed "autoallergy" and is ongoing discussed regarding its impact on the disease. Since severely affected patients tend to develop IgE-hypersensitivity reactions to numerous environmental allergens, the impact of immune responses to self-proteins is difficult to determine. On the other hand: any autoreactivity, irrespective of the magnitude, implicates the potential of driving the chronification of the disease while shaping the immune response. This review article revisits the observations made on autoallergy from an actual point of view and tries to approach the question whether these still point to a contribution to the disease.

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References
1.
Mayer C, Appenzeller U, Seelbach H, Achatz G, Oberkofler H, Breitenbach M . Humoral and cell-mediated autoimmune reactions to human acidic ribosomal P2 protein in individuals sensitized to Aspergillus fumigatus P2 protein. J Exp Med. 1999; 189(9):1507-12. PMC: 2193053. DOI: 10.1084/jem.189.9.1507. View

2.
Ohkouchi K, Mizutani H, Tanaka M, Takahashi M, Nakashima K, Shimizu M . Anti-elongation factor-1alpha autoantibody in adult atopic dermatitis patients. Int Immunol. 1999; 11(10):1635-40. DOI: 10.1093/intimm/11.10.1635. View

3.
Arstila T, Casrouge A, Baron V, Even J, Kanellopoulos J, Kourilsky P . A direct estimate of the human alphabeta T cell receptor diversity. Science. 1999; 286(5441):958-61. DOI: 10.1126/science.286.5441.958. View

4.
RAMMENSEE H, Bachmann J, Emmerich N, Bachor O, Stevanovic S . SYFPEITHI: database for MHC ligands and peptide motifs. Immunogenetics. 1999; 50(3-4):213-9. DOI: 10.1007/s002510050595. View

5.
de Visser K, Cordaro T, Kioussis D, Haanen J, Schumacher T, Kruisbeek A . Tracing and characterization of the low-avidity self-specific T cell repertoire. Eur J Immunol. 2000; 30(5):1458-68. DOI: 10.1002/(SICI)1521-4141(200005)30:5<1458::AID-IMMU1458>3.0.CO;2-2. View