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2018 ; 9
(ä): 689
Nephropedia Template TP
Maurer M
; Altrichter S
; Schmetzer O
; Scheffel J
; Church MK
; Metz M
Front Immunol
2018[]; 9
(ä): 689
PMID29686678
show ga
The study of autoimmunity mediated by immunoglobulin E (IgE) autoantibodies,
which may be termed autoallergy, is in its infancy. It is now recognized that
systemic lupus erythematosus, bullous pemphigoid (BP), and chronic urticaria,
both spontaneous and inducible, are most likely to be mediated, at least in part,
by IgE autoantibodies. The situation in other conditions, such as autoimmune
uveitis, rheumatoid arthritis, hyperthyroid Graves' disease, autoimmune
pancreatitis, and even asthma, is far less clear but evidence for autoallergy is
accumulating. To be certain of an autoallergic mechanism, it is necessary to
identify both IgE autoantibodies and their targets as has been done with the
transmembrane protein BP180 and the intracellular protein BP230 in BP and IL-24
in chronic spontaneous urticaria. Also, IgE-targeted therapies, such as anti-IgE,
must have been shown to be of benefit to patients as has been done with both of
these conditions. This comprehensive review of the literature on IgE-mediated
autoallergy focuses on three related questions. What do we know about the
prevalence of IgE autoantibodies and their targets in different diseases? What do
we know about the relevance of IgE autoantibodies in different diseases? What do
we know about the cellular and molecular effects of IgE autoantibodies? In
addition to providing answers to these questions, based on a broad review of the
literature, we outline the current gaps of knowledge in our understanding of IgE
autoantibodies and describe approaches to address them.
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