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Goncalves et al. Neuroimmunol Neuroinflammation 2019;6:6 Neuroimmunology and
DOI: 10.20517/2347-8659.2019.08 Neuroinflammation

Letter to Editor Open Access

The involvement of anti-neurofascin 155 antibodies in
central and peripheral demyelinating diseases

Marcus Vinicius Magno Goncalves , Yara Dadalti Fragoso 2
1
1 Department of Neurology, Universidade da Regiao de Joinville, Joinville, SC 89219-710, Brazil.
2 Universidade Metropolitana de Santos, MS & Headache Research, Santos, SP 11045-002, Brazil.

Correspondence to: Dr. Yara Dadalti Fragoso, Department of Neurology, Medical School, UNIMES, Avenida Conselheiro Nebias 536,
Santos, SP 11045-002, Brazil. E-mail: yara@bsnet.com.br
How to cite this article: Goncalves MVM, Fragoso YD. The involvement of anti-neurofascin 155 antibodies in central and peripheral
demyelinating diseases. Neuroimmunol Neuroinflammation 2019;6:6. http://dx.doi.org/10.20517/2347-8659.2019.08
Received: 16 Feb 2019 Accepted: 28 Feb 2019 Published: 8 Apr 2019

Science Editor: Athanassios P. Kyritsis Copy Editor: Cai-Hong Wang Production Editor: Huan-Liang Wu

The immunological aspects of autoantibodies directed against paranodal and nodal proteins form a
prominent field of research. Contactin-1 and contactin-1 associated protein, gliomedin and neurofascin
[1,2]
(NF) are Ranvier node-related proteins . Antibodies against these proteins have been identified in
chronic demyelinating conditions, such as multiple sclerosis (MS) and chronic inflammatory demyelinating
[3,4]
polyradiculoneuropathy (CIDP); and in acute demyelinating diseases such as Guillain-Barre syndrome .
Myelin and the paranodal axoglial junctions flanking the nodes of Ranvier are not merely passive
transmitters of electric signals: instead, they have essential roles in maintaining the structural integrity of
[5]
myelin-axolemmal interactions, bidirectional signaling and regulation of ion channels .
[6]
Here, we will focus on NF155, a major constituent of the Ranvier paranodal junction . NF155 belongs to
the L1 family of transmembrane cell adhesion molecules [Figure 1], typically presenting an evolutionary
well-conserved protein domain structure with six immunoglobulin and five fibronectin type III domains,
[7,8]
a transmembrane domain and a cytoplasmic domain with 113 amino acids . It is expressed at paranodes
[9]
by terminal loops of myelin and its main function is to stabilize these paranodes. Other isoforms of NFs
(NF166, NF180 and NF186) are equally involved in dynamic mechanisms of synaptic stabilization, neural
[7]
outgrowth and clustering of sodium channels .

Patients with CIDP who present antibodies against NF155 have a particular disease course that involves
onset at younger age, tremors, ataxia, dysarthria, nystagmus, extremely high protein levels in spinal fluid,
symmetrical spinal root and plexus hypertrophy [10,11] . In addition, over 70% of these patients can have
[10]
abnormal visual-evoked potentials during the course of CIDP . CIDP patients with anti-NF155 antibodies

© The Author(s) 2019. Open Access This article is licensed under a Creative Commons Attribution 4.0
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