Terminal complement activation is increased and associated with disease severity in CIDP

Terminal complement activation is increased and associated with disease severity in CIDP

Chronic inflammatory demyelinating polyneuropathy (CIDP) is the most common chronic autoimmune neuropathy. While both cell‐mediated and humoral mechanisms contribute to its pathogenesis, the rapid clinical response to plasmapheresis implicates a circulating factor responsible for peripheral nerve in...

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Main Authors: Quast, Isaak, Keller, Christian W., Hiepe, Falk, Tackenberg, Björn, Lünemann, Jan D.
Format: Online
Language:English
Published: John Wiley and Sons Inc. 2016
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5018585/
id pubmed-5018585
recordtype oai_dc
spelling pubmed-50185852016-09-19 Terminal complement activation is increased and associated with disease severity in CIDP Quast, Isaak Keller, Christian W. Hiepe, Falk Tackenberg, Björn Lünemann, Jan D. Brief Communications Chronic inflammatory demyelinating polyneuropathy (CIDP) is the most common chronic autoimmune neuropathy. While both cell‐mediated and humoral mechanisms contribute to its pathogenesis, the rapid clinical response to plasmapheresis implicates a circulating factor responsible for peripheral nerve injury. We report that treatment‐naïve patients with CIDP show increased serum and CSF levels of the anaphylatoxin C5a and the soluble terminal complement complex (sTCC). Systemic terminal complement activation correlates with clinical disease severity as determined by the Inflammatory Neuropathy Cause and Treatment (INCAT) disability scale. These data indicate that complement activation contributes to peripheral nerve injury and suggest that complement inhibition should be explored for its potential therapeutic merit in CIDP. John Wiley and Sons Inc. 2016-07-25 /pmc/articles/PMC5018585/ /pubmed/27648461 http://dx.doi.org/10.1002/acn3.331 Text en © 2016 The Authors. Annals of Clinical and Translational Neurology published by Wiley Periodicals, Inc on behalf of American Neurological Association. This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs (http://creativecommons.org/licenses/by-nc-nd/4.0/) License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Quast, Isaak
Keller, Christian W.
Hiepe, Falk
Tackenberg, Björn
Lünemann, Jan D.
spellingShingle Quast, Isaak
Keller, Christian W.
Hiepe, Falk
Tackenberg, Björn
Lünemann, Jan D.
Terminal complement activation is increased and associated with disease severity in CIDP
author_facet Quast, Isaak
Keller, Christian W.
Hiepe, Falk
Tackenberg, Björn
Lünemann, Jan D.
author_sort Quast, Isaak
title Terminal complement activation is increased and associated with disease severity in CIDP
title_short Terminal complement activation is increased and associated with disease severity in CIDP
title_full Terminal complement activation is increased and associated with disease severity in CIDP
title_fullStr Terminal complement activation is increased and associated with disease severity in CIDP
title_full_unstemmed Terminal complement activation is increased and associated with disease severity in CIDP
title_sort terminal complement activation is increased and associated with disease severity in cidp
description Chronic inflammatory demyelinating polyneuropathy (CIDP) is the most common chronic autoimmune neuropathy. While both cell‐mediated and humoral mechanisms contribute to its pathogenesis, the rapid clinical response to plasmapheresis implicates a circulating factor responsible for peripheral nerve injury. We report that treatment‐naïve patients with CIDP show increased serum and CSF levels of the anaphylatoxin C5a and the soluble terminal complement complex (sTCC). Systemic terminal complement activation correlates with clinical disease severity as determined by the Inflammatory Neuropathy Cause and Treatment (INCAT) disability scale. These data indicate that complement activation contributes to peripheral nerve injury and suggest that complement inhibition should be explored for its potential therapeutic merit in CIDP.
publisher John Wiley and Sons Inc.
publishDate 2016
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5018585/
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