Neuromyelitis optica: Passive transfer to rats by human immunoglobulin

Makoto Kinoshita; Yuji Nakatsuji; Takashi Kimura; Masayuki Moriya; Kazushiro Takata; Tatsusada Okuno; Atsushi Kumanogoh; Koji Kajiyama; Hiroo Yoshikawa; Saburo Sakoda

doi:10.1016/j.bbrc.2009.06.085

Neuromyelitis optica: Passive transfer to rats by human immunoglobulin

Makoto Kinoshita, Yuji Nakatsuji^*, Takashi Kimura, Masayuki Moriya, Kazushiro Takata, Tatsusada Okuno, Atsushi Kumanogoh, Koji Kajiyama, Hiroo Yoshikawa, Saburo Sakoda

^*Corresponding author for this work

Neurology

Research output: Contribution to journal › Article › peer-review

224 Scopus citations

Abstract

Recurrent attacks of optic neuritis and myelitis are the hallmarks of both neuromyelitis optica (NMO) and multiple sclerosis (MS). NMO immunoglobulin G (NMO-IgG), which recognizes astrocytic aquaporin-4 (AQP4) water channels, is a specific serum autoantibody that distinguishes NMO from MS. The pathogenic role of the anti-AQP4 antibody (AQP4-Ab, NMO-IgG) in NMO has been speculated based on several studies in vitro. The aim of this study was to demonstrate the pathogenicity of AQP4-Ab in vivo. We obtained IgG from patients who underwent therapeutic plasmapheresis, and developed an animal model by passive transfer of IgG to rats. The active lesions of the rats exhibited pathological characteristics strikingly similar to those of NMO, marked by astrocytic loss and perivascular deposition of immunoglobulin and complements. These findings provide the first evidence of the pathogenicity of AQP4-Ab in vivo and support the therapeutic efficacy of eliminating the antibodies by plasmapheresis.

Original language	English
Pages (from-to)	623-627
Number of pages	5
Journal	Biochemical and Biophysical Research Communications
Volume	386
Issue number	4
DOIs	https://doi.org/10.1016/j.bbrc.2009.06.085
State	Published - 2009/09/04

Keywords

Animal model
Aquaporin-4
Astrocyte
Complement
Experimental autoimmune encephalomyelitis
Multiple sclerosis
Neuromyelitis optica
Passive transfer

ASJC Scopus subject areas

Biophysics
Biochemistry
Molecular Biology
Cell Biology

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@article{757129962c8443149b35aebe48a491ac,

title = "Neuromyelitis optica: Passive transfer to rats by human immunoglobulin",

abstract = "Recurrent attacks of optic neuritis and myelitis are the hallmarks of both neuromyelitis optica (NMO) and multiple sclerosis (MS). NMO immunoglobulin G (NMO-IgG), which recognizes astrocytic aquaporin-4 (AQP4) water channels, is a specific serum autoantibody that distinguishes NMO from MS. The pathogenic role of the anti-AQP4 antibody (AQP4-Ab, NMO-IgG) in NMO has been speculated based on several studies in vitro. The aim of this study was to demonstrate the pathogenicity of AQP4-Ab in vivo. We obtained IgG from patients who underwent therapeutic plasmapheresis, and developed an animal model by passive transfer of IgG to rats. The active lesions of the rats exhibited pathological characteristics strikingly similar to those of NMO, marked by astrocytic loss and perivascular deposition of immunoglobulin and complements. These findings provide the first evidence of the pathogenicity of AQP4-Ab in vivo and support the therapeutic efficacy of eliminating the antibodies by plasmapheresis.",

keywords = "Animal model, Aquaporin-4, Astrocyte, Complement, Experimental autoimmune encephalomyelitis, Multiple sclerosis, Neuromyelitis optica, Passive transfer",

author = "Makoto Kinoshita and Yuji Nakatsuji and Takashi Kimura and Masayuki Moriya and Kazushiro Takata and Tatsusada Okuno and Atsushi Kumanogoh and Koji Kajiyama and Hiroo Yoshikawa and Saburo Sakoda",

note = "Funding Information: We thank Dr. Tomoyuki Sugimoto for expert statistical assistance and Dr. Keiko Tanaka for the serum AQP4-Ab test. This study was supported in part by the Program of Fundamental Studies in Health Sciences of the National Institute of Biomedical Innovation (NIBIO) and by Health and Labour Sciences Research Grants for research on intractable diseases from Ministry of Health, Labour and Welfare of Japan. ",

year = "2009",

month = sep,

day = "4",

doi = "10.1016/j.bbrc.2009.06.085",

language = "英語",

volume = "386",

pages = "623--627",

journal = "Biochemical and Biophysical Research Communications",

issn = "0006-291X",

publisher = "Elsevier B.V.",

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}

TY - JOUR

T1 - Neuromyelitis optica

T2 - Passive transfer to rats by human immunoglobulin

AU - Kinoshita, Makoto

AU - Nakatsuji, Yuji

AU - Kimura, Takashi

AU - Moriya, Masayuki

AU - Takata, Kazushiro

AU - Okuno, Tatsusada

AU - Kumanogoh, Atsushi

AU - Kajiyama, Koji

AU - Yoshikawa, Hiroo

AU - Sakoda, Saburo

N1 - Funding Information: We thank Dr. Tomoyuki Sugimoto for expert statistical assistance and Dr. Keiko Tanaka for the serum AQP4-Ab test. This study was supported in part by the Program of Fundamental Studies in Health Sciences of the National Institute of Biomedical Innovation (NIBIO) and by Health and Labour Sciences Research Grants for research on intractable diseases from Ministry of Health, Labour and Welfare of Japan.

PY - 2009/9/4

Y1 - 2009/9/4

N2 - Recurrent attacks of optic neuritis and myelitis are the hallmarks of both neuromyelitis optica (NMO) and multiple sclerosis (MS). NMO immunoglobulin G (NMO-IgG), which recognizes astrocytic aquaporin-4 (AQP4) water channels, is a specific serum autoantibody that distinguishes NMO from MS. The pathogenic role of the anti-AQP4 antibody (AQP4-Ab, NMO-IgG) in NMO has been speculated based on several studies in vitro. The aim of this study was to demonstrate the pathogenicity of AQP4-Ab in vivo. We obtained IgG from patients who underwent therapeutic plasmapheresis, and developed an animal model by passive transfer of IgG to rats. The active lesions of the rats exhibited pathological characteristics strikingly similar to those of NMO, marked by astrocytic loss and perivascular deposition of immunoglobulin and complements. These findings provide the first evidence of the pathogenicity of AQP4-Ab in vivo and support the therapeutic efficacy of eliminating the antibodies by plasmapheresis.

AB - Recurrent attacks of optic neuritis and myelitis are the hallmarks of both neuromyelitis optica (NMO) and multiple sclerosis (MS). NMO immunoglobulin G (NMO-IgG), which recognizes astrocytic aquaporin-4 (AQP4) water channels, is a specific serum autoantibody that distinguishes NMO from MS. The pathogenic role of the anti-AQP4 antibody (AQP4-Ab, NMO-IgG) in NMO has been speculated based on several studies in vitro. The aim of this study was to demonstrate the pathogenicity of AQP4-Ab in vivo. We obtained IgG from patients who underwent therapeutic plasmapheresis, and developed an animal model by passive transfer of IgG to rats. The active lesions of the rats exhibited pathological characteristics strikingly similar to those of NMO, marked by astrocytic loss and perivascular deposition of immunoglobulin and complements. These findings provide the first evidence of the pathogenicity of AQP4-Ab in vivo and support the therapeutic efficacy of eliminating the antibodies by plasmapheresis.

KW - Animal model

KW - Aquaporin-4

KW - Astrocyte

KW - Complement

KW - Experimental autoimmune encephalomyelitis

KW - Multiple sclerosis

KW - Neuromyelitis optica

KW - Passive transfer

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U2 - 10.1016/j.bbrc.2009.06.085

DO - 10.1016/j.bbrc.2009.06.085

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SN - 0006-291X

VL - 386

SP - 623

EP - 627

JO - Biochemical and Biophysical Research Communications

JF - Biochemical and Biophysical Research Communications

IS - 4

ER -

Neuromyelitis optica: Passive transfer to rats by human immunoglobulin

Abstract

Keywords

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