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The Intersection of IgE Autoantibodies and Eosinophilia in the Pathogenesis of Bullous Pemphigoid
Journal article   Open access   Peer reviewed

The Intersection of IgE Autoantibodies and Eosinophilia in the Pathogenesis of Bullous Pemphigoid

Kelly N. Messingham, Tyler P. Crowe and Janet A. Fairley
Frontiers in immunology, Vol.10, pp.2331-2331
10/04/2019
DOI: 10.3389/fimmu.2019.02331
PMCID: PMC6787172
PMID: 31636640
url
https://doi.org/10.3389/fimmu.2019.02331View
Published (Version of record) Open Access

Abstract

Bullous pemphigoid (BP) is an autoimmune blistering disease characterized by autoantibodies targeting cellular adhesion molecules. While IgE autoantibodies are occasionally reported in other autoimmune blistering diseases, BP is unique in that most BP patients develop an IgE autoantibody response. It is not known why BP patients develop self-reactive IgE and the precise role of IgE in BP pathogenesis is not fully understood. However, clinical evidence suggests an association between elevated IgE antibodies and eosinophilia in BP patients. Since eosinophils are multipotent effector cells, capable cytotoxicity and immune modulation, the putative interaction between IgE and eosinophils is a primary focus in current studies aimed at understanding the key components of disease pathogenesis. In this review, we provide an overview of BP pathogenesis, highlighting clinical and experimental evidence supporting central roles for IgE and eosinophils as independent mediators of disease and via their interaction. Additionally, therapeutics targeting IgE, the Th2 axis, or eosinophils are also discussed.
autoantibody autoimmunity blister Bullous pemphigoid collagen XVII eosinophil IgE Immunology skin

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