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Article ; Online: Neurofascin-155 IgG4 in chronic inflammatory demyelinating polyneuropathy.

Devaux, Jérôme J / Miura, Yumako / Fukami, Yuki / Inoue, Takayuki / Manso, Constance / Belghazi, Maya / Sekiguchi, Kenji / Kokubun, Norito / Ichikawa, Hiroo / Wong, Anna Hiu Yi / Yuki, Nobuhiro

Neurology

2016 Volume 86, Issue 9, Page(s) 800–807

Abstract: ... inflammatory demyelinating polyneuropathy (CIDP) displaying anti-neurofascin-155 (NF155) immunoglobulin G4 ... IgG antibodies targeted similarly central and peripheral paranodes.: Conclusion: Anti-NF155 IgG4 ... IgG4) antibodies.: Methods: In sera from 533 patients with CIDP, anti-NF155 IgG4 antibodies were ...

Abstract	Objective: We report the clinical and serologic features of Japanese patients with chronic inflammatory demyelinating polyneuropathy (CIDP) displaying anti-neurofascin-155 (NF155) immunoglobulin G4 (IgG4) antibodies. Methods: In sera from 533 patients with CIDP, anti-NF155 IgG4 antibodies were detected by ELISA. Binding of IgG antibodies to central and peripheral nerves was tested. Results: Anti-NF155 IgG4 antibodies were identified in 38 patients (7%) with CIDP, but not in disease controls or normal participants. These patients were younger at onset as compared to 100 anti-NF155-negative patients with CIDP. Twenty-eight patients (74%) presented with sensory ataxia, 16 (42%) showed tremor, 5 (13%) presented with cerebellar ataxia associated with nystagmus, 3 (8%) had demyelinating lesions in the CNS, and 20 of 25 (80%) had poor response to IV immunoglobulin. The clinical features of the antibody-positive patients were statistically more frequent as compared to negative patients with CIDP (n = 100). Anti-NF155 IgG antibodies targeted similarly central and peripheral paranodes. Conclusion: Anti-NF155 IgG4 antibodies were associated with a subgroup of patients with CIDP showing a younger age at onset, ataxia, tremor, CNS demyelination, and a poor response to IV immunoglobulin. The autoantibodies may serve as a biomarker to improve patients' diagnosis and guide treatments.
MeSH term(s)	Adolescent ; Adult ; Age Distribution ; Aged ; Aged, 80 and over ; Autoantibodies/blood ; Autoantibodies/immunology ; Biomarkers/blood ; Cell Adhesion Molecules/blood ; Cell Adhesion Molecules/immunology ; Child ; Female ; Humans ; Immunoglobulin G/blood ; Immunoglobulin G/immunology ; Incidence ; Japan/epidemiology ; Male ; Middle Aged ; Nerve Growth Factors/blood ; Nerve Growth Factors/immunology ; Polyradiculoneuropathy, Chronic Inflammatory Demyelinating/blood ; Polyradiculoneuropathy, Chronic Inflammatory Demyelinating/diagnosis ; Polyradiculoneuropathy, Chronic Inflammatory Demyelinating/epidemiology ; Risk Assessment/methods ; Young Adult
Chemical Substances	Autoantibodies ; Biomarkers ; Cell Adhesion Molecules ; Immunoglobulin G ; NFASC protein, human ; Nerve Growth Factors
Language	English
Publishing date	2016-03-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	207147-2
ISSN	1526-632X ; 0028-3878
ISSN (online)	1526-632X
ISSN	0028-3878
DOI	10.1212/WNL.0000000000002418
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Article ; Online: Unique HLA haplotype associations in IgG4 anti-neurofascin 155 antibody-positive chronic inflammatory demyelinating polyneuropathy.

Ogata, Hidenori / Isobe, Noriko / Zhang, Xu / Yamasaki, Ryo / Fujii, Takayuki / Machida, Akira / Morimoto, Nobutoshi / Kaida, Kenichi / Masuda, Teruaki / Ando, Yukio / Kuwahara, Motoi / Kusunoki, Susumu / Nakamura, Yuri / Matsushita, Takuya / Kira, Jun-Ichi

Journal of neuroimmunology

2019 Volume 339, Page(s) 577139

Abstract: ... 155 (NF155) antibody-positive chronic inflammatory demyelinating polyneuropathy (CIDP), we genotyped ... To clarify the immunogenetic background of patients with immunoglobulin G (IgG)4 anti-neurofascin ... them with those of healthy Japanese controls. All IgG4 anti-NF155 antibody-positive CIDP patients exclusively carried ...

Abstract	To clarify the immunogenetic background of patients with immunoglobulin G (IgG)4 anti-neurofascin 155 (NF155) antibody-positive chronic inflammatory demyelinating polyneuropathy (CIDP), we genotyped the extended human leukocyte antigen (HLA) haplotypes in 22 Japanese patients with this disorder and compared them with those of healthy Japanese controls. All IgG4 anti-NF155 antibody-positive CIDP patients exclusively carried either HLA-DRB115:01-DRB501:01-DQA101:02-DQB106:02 or -(A24:02)-B52:01-C12:02-DRB115:02-DRB501:02-DQA101:03-DQB106:01, resulting in significantly increased HLA-DRB115, -DRB115:01, -DQB106:01/06:02, -DQB106:02, and -DRB115:01-DQB1*06:02 frequencies compared with healthy Japanese controls. These findings indicate the involvement of specific HLA class II molecules in the pathomechanisms of IgG4 anti-NF155 antibody-positive CIDP.
MeSH term(s)	Adolescent ; Adult ; Aged ; Asian Continental Ancestry Group/genetics ; Autoantibodies/blood ; Autoantibodies/genetics ; Cell Adhesion Molecules/blood ; Cell Adhesion Molecules/genetics ; Female ; HLA Antigens/blood ; HLA Antigens/genetics ; Haplotypes/genetics ; Humans ; Immunoglobulin G/blood ; Immunoglobulin G/genetics ; Male ; Middle Aged ; Nerve Growth Factors/blood ; Nerve Growth Factors/genetics ; Polyradiculoneuropathy, Chronic Inflammatory Demyelinating/blood ; Polyradiculoneuropathy, Chronic Inflammatory Demyelinating/diagnosis ; Polyradiculoneuropathy, Chronic Inflammatory Demyelinating/genetics ; Young Adult
Chemical Substances	Autoantibodies ; Cell Adhesion Molecules ; HLA Antigens ; Immunoglobulin G ; NFASC protein, human ; Nerve Growth Factors
Language	English
Publishing date	2019-12-16
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	8335-5
ISSN	1872-8421 ; 0165-5728
ISSN (online)	1872-8421
ISSN	0165-5728
DOI	10.1016/j.jneuroim.2019.577139
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Article: Clinical Features of Autoimmune Nodopathy With Anti-Neurofascin-155 Antibodies in South Koreans.

Lyou, Hyun Ji / Chung, Yeon Hak / Kim, Min Ju / Kim, MinGi / Jeon, Mi Young / Kim, Seung Woo / Shin, Ha Young / Kim, Byoung Joon

Journal of clinical neurology (Seoul, Korea)

2024 Volume 20, Issue 2, Page(s) 186–193

Abstract: ... the diagnostic criteria for chronic inflammatory demyelinating polyneuropathy (CIDP) were tested for anti-NF155 ... Background and purpose: Anti-neurofascin-155 (NF155) antibody is one of the autoantibodies ... patients was also positive for anti-NF186 and anti-NF140 antibodies. IgG4 was the predominant subclass ...

Abstract	Background and purpose: Anti-neurofascin-155 (NF155) antibody is one of the autoantibodies associated with autoimmune nodopathy. We aimed to determine the clinical features of South Korean patients with anti-NF155-antibody-positive autoimmune nodopathy. Methods: The sera of 68 patients who fulfilled the diagnostic criteria for chronic inflammatory demyelinating polyneuropathy (CIDP) were tested for anti-NF155 antibodies using a cell-based assay (CBA) and enzyme-linked immunosorbent assay (ELISA). The anti-NF155-positive sera were also assayed for NF155 immunoglobulin G (IgG) subclasses, and for anti-NF186 and NF140 antibodies. The clinical features of the patients were reviewed retrospectively. Results: Among the 68 patients, 6 (8.8%) were positive for anti-NF155 antibodies in both the CBA and ELISA. One of those six patients was also positive for anti-NF186 and anti-NF140 antibodies. IgG4 was the predominant subclass in four patients. The mean age at onset was 32.2 years. All six positive patients presented with progressive sensory ataxia. Five patients treated using corticosteroids presented a partial or no response. All six patients were treated using intravenous immunoglobulin (IVIg). Among them, five exhibited a partial or poor response and the other exhibited a good response. All three patients treated using rituximab showed a good response. Conclusions: The clinical characteristics of the patients were consistent with those in previous studies. Anti-NF155 antibody assay is necessary for diagnosing autoimmune nodopathy and its appropriate treatment, especially in young patients with CIDP who present with sensory ataxia and poor therapeutic responses to corticosteroids and IVIg.
Language	English
Publishing date	2024-01-01
Publishing country	Korea (South)
Document type	Journal Article
ZDB-ID	2500489-X
ISSN	2005-5013 ; 1738-6586
ISSN (online)	2005-5013
ISSN	1738-6586
DOI	10.3988/jcn.2023.0055
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Article ; Online: Anti-neurofascin-155 antibody mediated a distinct phenotype of chronic inflammatory demyelinating polyradiculoneuropathy.

Zhang, Lijie / Zhang, Yuanyuan / Li, Runyun / Zhu, Jiting / Lin, Aiyu / Yan, Yaping / Zhang, Zaiqiang / Wang, Ning / Xu, Guorong / Fu, Ying

Journal of neurology

2024

Abstract: ... inflammatory demyelinating polyneuropathy (NF155: Results: In 368 plasma samples, 50 Ranvier's ... immune mechanisms underlying antibody generation.: Methods: Antibodies against anti-neurofascin-155 ... primarily IgG4 subclass, linked to CIDP features including early onset, tremor, sensory disturbance ...

Abstract	Background: To investigate Ranvier's autoantibodies prevalence and isotypes in various peripheral neuropathy variants, compare clinical features between seronegative and seropositive patients, and elucidate immune mechanisms underlying antibody generation. Methods: Antibodies against anti-neurofascin-155 (NF155), NF186, contactin-1 (CNTN1), CNTN2, contactin-associated protein 1 (CASPR1), and CASPR2 were identified through cell-based assays. Plasma cytokines were analyzed in anti-NF155 antibody-positive chronic inflammatory demyelinating polyneuropathy (NF155 Results: In 368 plasma samples, 50 Ranvier's autoantibodies were found in 45 individuals, primarily in CIDP cases (25 out of 69 patients) and in 10 out of 122 Guillain-Barré syndrome patients. Anti-NF155 and CNTN1-IgG were exclusive to CIDP. Fourteen samples were NF155-IgG, primarily IgG4 subclass, linked to CIDP features including early onset, tremor, sensory disturbance, elevated CSF protein, prolonged motor latency, conduction block, and poor treatment response. NF155-IgG had low sensitivity (20.28%) but high specificity (100%) for CIDP, rising to 88.88% with tremor and prolonged motor latency. Cytokine profiling in NF155 Conclusion: The study emphasizes the high specificity and sensitivity of NF155-IgG for diagnosing CIDP characterized by distinctive features. Further investigation into circulating NF155-specific B cell phenotypes may pave the way for B cell directed therapy.
Language	English
Publishing date	2024-05-21
Publishing country	Germany
Document type	Journal Article
ZDB-ID	187050-6
ISSN	1432-1459 ; 0340-5354 ; 0012-1037 ; 0939-1517 ; 1619-800X
ISSN (online)	1432-1459
ISSN	0340-5354 ; 0012-1037 ; 0939-1517 ; 1619-800X
DOI	10.1007/s00415-024-12443-9
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Article ; Online: IgG4 Valency Modulates the Pathogenicity of Anti-Neurofascin-155 IgG4 in Autoimmune Nodopathy.

Jentzer, Alexandre / Attal, Arthur / Roué, Clémence / Raymond, Julie / Lleixà, Cinta / Illa, Isabel / Querol, Luis / Taieb, Guillaume / Devaux, Jérôme

Neurology(R) neuroimmunology & neuroinflammation

2022 Volume 9, Issue 5

Abstract: ... with a subgroup of patients with chronic inflammatory demyelinating polyneuropathy (CIDP), currently named ... Background and objectives: IgG4 autoantibodies to neurofascin-155 (Nfasc155) are associated ... axons by inducing Nfasc155 depletion and paranode destruction. In blood, IgG4 have the potency ...

Abstract	Background and objectives: IgG4 autoantibodies to neurofascin-155 (Nfasc155) are associated with a subgroup of patients with chronic inflammatory demyelinating polyneuropathy (CIDP), currently named autoimmune nodopathy. We previously demonstrated that those antibodies alter conduction along myelinated axons by inducing Nfasc155 depletion and paranode destruction. In blood, IgG4 have the potency to exchange their moiety with other unrelated IgG4 through a process called Fab-arm exchange (FAE). This process results in functionally monovalent antibodies and may affect the pathogenicity of autoantibodies. Here, we examined this issue and whether FAE is beneficial or detrimental for Nfasc155 autoimmune nodopathy. Methods: The bivalency and monospecificity of anti-Nfasc155 were examined by sandwich ELISA in 10 reactive patients, 10 unreactive CIDP patients, and 10 healthy controls. FAE was induced in vitro using reduced glutathione and unreactive IgG4, and the ratio of the κ:λ light chain was monitored. To determine the pathogenic potential of bivalent anti-Nfasc155 IgG4, autoantibodies derived from patients were enzymatically cleaved into monovalent Fab and bivalent F(ab') Results: Monospecific bivalent IgG4 against Nfasc155 were detected in the serum of all reactive patients, indicating that a fraction of IgG4 have not undergone FAE in situ. These IgG4 were, nonetheless, capable of engaging into FAE with unreactive IgG4 in vitro, and this decreased the levels of monospecific antibodies and modulated the ratio of the κ:λ light chain. When injected in animals, monovalent anti-Nfasc155 Fab did not alter the formation of paranodes; by contrast, both native anti-Nfasc155 IgG4 and F(ab') Discussion: Our findings demonstrate that monospecific and bivalent anti-Nfasc155 IgG4 are detected in patients and that those autoantibodies are the pathogenic ones. The transformation of anti-Nfasc155 IgG4 into monovalent Fab or functionally monovalent IgG4 through FAE strongly decreases paranodal alterations. Bivalency thus appears crucial for Nfasc155 clustering and paranode destruction.
MeSH term(s)	Animals ; Autoantibodies ; Cell Adhesion Molecules ; Immunoglobulin G ; Nerve Growth Factors ; Polyradiculoneuropathy, Chronic Inflammatory Demyelinating ; Virulence
Chemical Substances	Autoantibodies ; Cell Adhesion Molecules ; Immunoglobulin G ; Nerve Growth Factors
Language	English
Publishing date	2022-08-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2767740-0
ISSN	2332-7812 ; 2332-7812
ISSN (online)	2332-7812
ISSN	2332-7812
DOI	10.1212/NXI.0000000000200014
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Article: Optic Nerve Demyelination in IgG4 Anti-Neurofascin 155 Antibody-Positive Combined Central and Peripheral Demyelination Syndrome.

Verghese, Alice / Krishnan, Dhayalan / Chia, Yuen Kang / Querol, Luis / Hiew, Fu Liong

Journal of central nervous system disease

2021 Volume 13, Page(s) 11795735211039913

Abstract: ... between multiple sclerosis (MS) and chronic inflammatory demyelinating polyneuropathy (CIDP). Of interest ... neurofascin 155 (anti-NF 155) also reported optic nerve dysfunction. We aimed to evaluate optic nerve ... demyelination among anti-NF 155 CIDP patients. We studied 2 patients with anti-NF 155 CIDP using ...

Abstract	Optic nerve demyelination is one of the clinical features of combined central and peripheral demyelination (CCPD), an entity with heterogenous immunopathogenesis and clinical characteristics, overlapping between multiple sclerosis (MS) and chronic inflammatory demyelinating polyneuropathy (CIDP). Of interest, earlier studies among patients with CIDP prior to discovery of antibodies against paranodal protein neurofascin 155 (anti-NF 155) also reported optic nerve dysfunction. We aimed to evaluate optic nerve demyelination among anti-NF 155 CIDP patients. We studied 2 patients with anti-NF 155 CIDP using visual-evoked potentials (VEP) and optical coherence tomography (OCT). Both patients had distal acquired demyelinating symmetric (DADS) subtype CIDP. Other common features were prominent sensory ataxia, hand tremors, significantly elevated cerebral spinal fluid protein, high titre anti-NF 155 antibodies and poor response to corticosteroid and intravenous immunoglobulin (IVIg). No central nervous system neuroradiological abnormality detected. Both had normal visual acuity and colour vision, but one had subclinical right relative afferent pupillary defect (RAPD). VEP of both showed bilateral prolonged P100 latencies. OCT for patient with RAPD demonstrated moderate to severe retinal nerve fibre layer (RNFL) thinning. Identification of optic nerve demyelination among subclinical CIDP with anti-NF 155 antibodies expanded the spectrum of demyelination within the subset of CCPD.
Language	English
Publishing date	2021-12-06
Publishing country	United States
Document type	Journal Article
ZDB-ID	2586873-1
ISSN	1179-5735
ISSN	1179-5735
DOI	10.1177/11795735211039913
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Article ; Online: Anti-Neurofascin-155 IgG4 antibodies prevent paranodal complex formation in vivo.

Manso, Constance / Querol, Luis / Lleixà, Cinta / Poncelet, Mallory / Mekaouche, Mourad / Vallat, Jean-Michel / Illa, Isabel / Devaux, Jérôme J

The Journal of clinical investigation

2019 Volume 129, Issue 6, Page(s) 2222–2236

Abstract: ... against Nfasc155 are implicated in the pathogenesis of chronic inflammatory demyelinating polyneuropathy ... Neurofascin-155 (Nfasc155) is an essential glial cell adhesion molecule expressed in paranodal ... results in the loss of septate-like junctions and in conduction slowing. In humans, IgG4 antibodies ...

Abstract	Neurofascin-155 (Nfasc155) is an essential glial cell adhesion molecule expressed in paranodal septate-like junctions of peripheral and central myelinated axons. The genetic deletion of Nfasc155 results in the loss of septate-like junctions and in conduction slowing. In humans, IgG4 antibodies against Nfasc155 are implicated in the pathogenesis of chronic inflammatory demyelinating polyneuropathy (CIDP). These antibodies are associated with an aggressive onset, a refractoriness to intravenous immunoglobulin, and tremor of possible cerebellar origin. Here, we examined the pathogenic effects of patient-derived anti-Nfasc155 IgG4. These antibodies did not inhibit the ability of Nfasc155 to complex with its axonal partners contactin-1/CASPR1 or induce target internalization. Passive transfer experiments revealed that IgG4 antibodies target Nfasc155 on Schwann cell surface, and diminished Nfasc155 protein levels and prevented paranodal complex formation in neonatal animals. In adult animals, chronic intrathecal infusions of antibodies also induced the loss of Nfasc155 and of paranodal specialization and resulted in conduction alterations in motor nerves. These results indicate that anti-Nfasc155 IgG4 perturb conduction in absence of demyelination, validating the existence of paranodopathy. These results also shed light on the mechanisms regulating protein insertion at paranodes.
MeSH term(s)	Animals ; Axons/immunology ; Axons/pathology ; Cell Adhesion Molecules/antagonists & inhibitors ; Cell Adhesion Molecules/immunology ; Chronic Disease ; Female ; HEK293 Cells ; Humans ; Immunoglobulin G/immunology ; Immunoglobulin G/pharmacology ; Male ; Motor Neurons/immunology ; Motor Neurons/pathology ; Nerve Growth Factors/antagonists & inhibitors ; Nerve Growth Factors/immunology ; Polyneuropathies/drug therapy ; Polyneuropathies/immunology ; Polyneuropathies/pathology ; Polyradiculoneuropathy/drug therapy ; Polyradiculoneuropathy/immunology ; Polyradiculoneuropathy/pathology ; Rats ; Rats, Inbred Lew ; Schwann Cells/immunology ; Schwann Cells/pathology
Chemical Substances	Cell Adhesion Molecules ; Immunoglobulin G ; NFASC protein, human ; Nerve Growth Factors ; Nfasc protein, rat
Language	English
Publishing date	2019-03-14
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI124694
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Article ; Online: Intrathecal cytokine profile in neuropathy with anti-neurofascin 155 antibody.

Ogata, Hidenori / Zhang, Xu / Yamasaki, Ryo / Fujii, Takayuki / Machida, Akira / Morimoto, Nobutoshi / Kaida, Kenichi / Masuda, Teruaki / Ando, Yukio / Kuwahara, Motoi / Kusunoki, Susumu / Nakamura, Yuri / Matsushita, Takuya / Isobe, Noriko / Kira, Jun-Ichi

Annals of clinical and translational neurology

2019 Volume 6, Issue 11, Page(s) 2304–2316

Abstract: ... polyneuropathy (CIDP) patients with IgG4 anti-neurofascin 155 (NF155) antibodies (NF155: Methods: Twenty-eight ... Objective: To characterize the CSF cytokine profile in chronic inflammatory demyelinating ... upregulation of type 2 helper T (Th2) cell cytokines is characteristic of IgG4 NF155 ...

Abstract	Objective: To characterize the CSF cytokine profile in chronic inflammatory demyelinating polyneuropathy (CIDP) patients with IgG4 anti-neurofascin 155 (NF155) antibodies (NF155 Methods: Twenty-eight CSF cytokines/chemokines/growth factors were measured by multiplexed fluorescent immunoassay in 35 patients with NF155 Results: CSF CXCL8/IL-8, IL-13, TNF-α, CCL11/eotaxin, CCL2/MCP-1, and IFN-γ were significantly higher, while IL-1β, IL-1ra, and G-CSF were lower, in NF155 Interpretation: Intrathecal upregulation of type 2 helper T (Th2) cell cytokines is characteristic of IgG4 NF155
MeSH term(s)	Adolescent ; Adult ; Aged ; Aged, 80 and over ; Autoantibodies/immunology ; Autoantigens/immunology ; Cell Adhesion Molecules/immunology ; Child ; Cytokines/cerebrospinal fluid ; Female ; Humans ; Male ; Middle Aged ; Nerve Growth Factors/immunology ; Polyradiculoneuropathy, Chronic Inflammatory Demyelinating/cerebrospinal fluid ; Polyradiculoneuropathy, Chronic Inflammatory Demyelinating/immunology ; Young Adult
Chemical Substances	Autoantibodies ; Autoantigens ; Cell Adhesion Molecules ; Cytokines ; NFASC protein, human ; Nerve Growth Factors
Language	English
Publishing date	2019-10-27
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2740696-9
ISSN	2328-9503 ; 2328-9503
ISSN (online)	2328-9503
ISSN	2328-9503
DOI	10.1002/acn3.50931
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Article ; Online: Autoantibodies to nodal isoforms of neurofascin in chronic inflammatory demyelinating polyneuropathy.

Delmont, Emilien / Manso, Constance / Querol, Luis / Cortese, Andrea / Berardinelli, Angela / Lozza, Alessandro / Belghazi, Maya / Malissart, Pauline / Labauge, Pierre / Taieb, Guillaume / Yuki, Nobuhiro / Illa, Isabel / Attarian, Shahram / Devaux, Jérôme J

Brain : a journal of neurology

2017 Volume 140, Issue 7, Page(s) 1851–1858

Abstract: ... compared to those with anti-neurofascin-155 IgG4. Most patients had a severe phenotype associated ... Chronic inflammatory demyelination polyneuropathy is a heterogeneous and treatable immune-mediated ... demonstrate that the pathogenic mechanisms responsible for chronic inflammatory demyelination polyneuropathy ...

Abstract	Chronic inflammatory demyelination polyneuropathy is a heterogeneous and treatable immune-mediated disorder that lacks biomarkers to support diagnosis. Recent evidence indicates that paranodal proteins (contactin 1, contactin-associated protein 1, and neurofascin-155) are the targets of autoantibodies in subsets of patients showing distinct clinical presentations. Here, we identified neurofascin-186 and neurofascin-140 as the main targets of autoantibodies in five patients presenting IgG reactivity against the nodes of Ranvier. Four patients displayed predominantly IgG4 antibodies, and one patient presented IgG3 antibodies that activated the complement pathway in vitro. These patients present distinct clinical features compared to those with anti-neurofascin-155 IgG4. Most patients had a severe phenotype associated with conduction block or decreased distal motor amplitude. Four patients had a subacute-onset and sensory ataxia. Two patients presented with nephrotic syndromes and one patient with an IgG4-related retroperitoneal fibrosis. Intravenous immunoglobulin and corticosteroids were effective in three patients, and one patient remitted following rituximab treatment. Clinical remission was associated with autoantibody depletion and with recovery of conduction block and distal motor amplitude suggesting a nodo-paranodopathy. Our data demonstrate that the pathogenic mechanisms responsible for chronic inflammatory demyelination polyneuropathy are broad and may include dysfunctions at the nodes of Ranvier in a subgroup of patients.
MeSH term(s)	Adolescent ; Adrenal Cortex Hormones/therapeutic use ; Adult ; Aged ; Aged, 80 and over ; Autoantibodies/blood ; Autoantibodies/immunology ; Case-Control Studies ; Cell Adhesion Molecules/immunology ; Child ; Child, Preschool ; Female ; Humans ; Immunoglobulins, Intravenous/therapeutic use ; Male ; Middle Aged ; Nerve Growth Factors/immunology ; Neural Conduction/physiology ; Polyradiculoneuropathy, Chronic Inflammatory Demyelinating/blood ; Polyradiculoneuropathy, Chronic Inflammatory Demyelinating/drug therapy ; Polyradiculoneuropathy, Chronic Inflammatory Demyelinating/immunology ; Protein Isoforms/immunology ; Ranvier's Nodes/immunology ; Rituximab/therapeutic use ; Young Adult
Chemical Substances	Adrenal Cortex Hormones ; Autoantibodies ; Cell Adhesion Molecules ; Immunoglobulins, Intravenous ; NFASC protein, human ; Nerve Growth Factors ; Protein Isoforms ; Rituximab (4F4X42SYQ6)
Language	English
Publishing date	2017-07-01
Publishing country	England
Document type	Journal Article
ZDB-ID	80072-7
ISSN	1460-2156 ; 0006-8950
ISSN (online)	1460-2156
ISSN	0006-8950
DOI	10.1093/brain/awx124
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Article: Anti-Neurofascin 155 Antibody-Positive Chronic Inflammatory Demyelinating Polyneuropathy/Combined Central and Peripheral Demyelination: Strategies for Diagnosis and Treatment Based on the Disease Mechanism.

Kira, Jun-Ichi

Frontiers in neurology

2021 Volume 12, Page(s) 665136

Abstract: Chronic inflammatory demyelinating polyneuropathy (CIDP) is an immune-mediated ... against nodal/paranodal proteins, such as neurofascin 155 (NF155), contactin 1, and contactin-associated ... protein 1. In most cases, the predominant immunoglobulin (IgG) subclass is IgG4. Node/paranode antibody ...

Abstract	Chronic inflammatory demyelinating polyneuropathy (CIDP) is an immune-mediated demyelinating disease of the peripheral nervous system (PNS). A small number of CIDP patients harbors autoantibodies against nodal/paranodal proteins, such as neurofascin 155 (NF155), contactin 1, and contactin-associated protein 1. In most cases, the predominant immunoglobulin (IgG) subclass is IgG4. Node/paranode antibody-positive CIDP demonstrates distinct features compared with antibody-negative CIDP, including a poor response to intravenous immunoglobulin. The neuropathology of biopsied sural nerve shows Schwann cell terminal loop detachment from axons without macrophage infiltration or inflammation. This is partly attributable to IgG4, which blocks protein-protein interactions without inducing inflammation. Anti-NF155 antibody-positive (NF155
Language	English
Publishing date	2021-06-10
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2564214-5
ISSN	1664-2295
ISSN	1664-2295
DOI	10.3389/fneur.2021.665136
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