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Skin Autoimmunity

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Front. Immunol. | doi: 10.3389/fimmu.2019.00627

Autoimmune Theories of Chronic Spontaneous Urticaria

Sonali Bracken1, Soman Abraham1 and  Amanda S. MacLeod1*
  • 1Duke University, United States

Urticaria (hives) is a highly prevalent skin disorder that can occur with or without associated angioedema. Chronic spontaneous urticaria (CSU) is a condition which persists for more than six weeks in duration and occurs in the absence of an identifiable provoking factor. CSU results from pathogenic activation of mast cells and basophils, which gives rise to the release of proinflammatory mediators that support the generation of urticaria. Several theories have been put forth regarding the pathogenesis of CSU with much evidence pointing towards a potential autoimmune etiology for this condition in up to 50% of patients with this condition. In this review, we highlight the evidence surrounding the autoimmune pathogenesis of chronic urticaria including recent data which suggests that CSU may involve contributions from both immunoglobin G (IgG)-specific and immunoglobulin E (IgE)-specific autoantibodies against a vast array of antigens that can span beyond those found on the surface of mast cells and basophils.

Keywords: Skin - immunology, mast cell, Urticaria, autoimmne disease, signaling, Innate & adaptive immune response, autoimminity, Innate immun system, anti-IgE, anti-FcER1, Autoallergy

Received: 23 Jan 2019; Accepted: 08 Mar 2019.

Edited by:

Ralf J. Ludwig, Universität zu Lübeck, Germany

Reviewed by:

Karoline Krause, Charité Medical University of Berlin, Germany
Martin Metz, Charité Medical University of Berlin, Germany  

Copyright: © 2019 Bracken, Abraham and MacLeod. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Dr. Amanda S. MacLeod, Duke University, Durham, 27708, North Carolina, United States, amanda.macleod@duke.edu