Research activity information

• Oct. 2024 日本神経免疫学会, Young Neuroimmunologist Award

• NMOSD: Adaptive Immunity Revisited

  Ritsu Akatani, Norio Chihara

  ABSTRACT Accumulating evidence underscores the pivotal role of adaptive immunity in the pathogenesis of AQP4‐IgG‐positive neuromyelitis optica spectrum disorder (NMOSD). Autoreactive B cells produce pathogenic antibodies against aquaporin‐4 (AQP4), and their dysregulation is evident in both peripheral blood and cerebrospinal fluid. These abnormalities include an increased frequency of plasmablasts and the expansion of atypical B‐cell subsets enriched for autoreactivity. Their activation and survival are supported by inflammatory cytokines such as interleukin‐6 (IL‐6), a key target of current immunotherapies. T‐cell subsets, including follicular helper T (Tfh) cells and Th17 cells, play essential roles by promoting B‐cell differentiation and amplifying inflammation. The interplay between B and T cells, together with cytokine dysregulation, constitutes a central immunopathogenic axis in NMOSD. Notably, some disease‐modifying therapies for multiple sclerosis have been shown to worsen NMOSD, suggesting fundamental differences in the underlying immune dynamics between the two diseases. This contrast highlights the need for disease‐specific therapeutic approaches and a deeper understanding of adaptive immune processes unique to NMOSD. Here, we revisit the immunopathogenesis of AQP4‐IgG‐positive NMOSD with a focus on adaptive immune mechanisms. We discuss current evidence on B‐ and T‐cell abnormalities, intrathecal immune responses, and how these insights have informed the development of targeted therapies.

  Lead, Wiley, Oct. 2025, Clinical and Experimental Neuroimmunology

  [Refereed][Invited]

  Scientific journal


• 神経変性と免疫 脳内常在性CD8陽性T細胞はアルツハイマー型認知症の超早期病態において脳内炎症環境を制御する

  辻 麻人, 千原 典夫, 赤谷 律, 刀坂 公崇, 西居 正汰, 上西 涼平, 眞鍋 達也, 齊藤 貴志, 西道 隆臣, 小林 千浩, 戸田 達史, 松本 理器

  (一社)日本神経免疫学会, Aug. 2025, 神経免疫学, 30(1) (1), 178 - 178, Japanese


• 多発性硬化症患者脳脊髄液のCD8+ T細胞上のPD-1発現上昇が良好な長期予後と相関する

  古東 秀介, 千原 典夫, 城間 京香, 辻 麻人, 刀坂 公崇, 西居 正汰, 的場 健人, 赤谷 律, 十河 正弥, 関口 兼司, 松本 理器

  (一社)日本神経学会, Oct. 2024, 臨床神経学, 64(Suppl.) (Suppl.), S236 - S236, Japanese


• 視神経脊髄炎スペクトラム障害の病態におけるIL-6阻害薬治療はB細胞をリバランスする

  赤谷 律, 千原 典夫, 原 敦, 辻 麻人, 古東 秀介, 城間 京香, 武田 涼輔, 刀坂 公崇, 西居 正汰, 松本 理器

  (一社)日本神経免疫学会, Oct. 2024, 神経免疫学, 29(1) (1), 173 - 173, Japanese


• NMOSD & MOGAD【WS2】髄液中central memory T細胞の増加が視神経脊髄炎(NMOSD)炎症発作時の重症度を予測する

  城間 京香, 千原 典夫, 武田 涼輔, 辻 麻人, 原 敦, 赤谷 律, 古東 秀介, 松本 理器

  (一社)日本神経免疫学会, Oct. 2024, 神経免疫学, 29(1) (1), 190 - 190, Japanese


• Interleukin-6 Signaling Blockade Induces Regulatory Plasmablasts in Neuromyelitis Optica Spectrum Disorder.

  Ritsu Akatani, Norio Chihara, Atsushi Hara, Asato Tsuji, Shusuke Koto, Kazuhiro Kobayashi, Tatsushi Toda, Riki Matsumoto

  BACKGROUND AND OBJECTIVES: Interleukin-6 receptor antibodies (IL-6R Abs), including satralizumab, are increasingly used to prevent relapse for neuromyelitis optica spectrum disorder (NMOSD). However, the detailed mechanism of action of this treatment on the lymphocyte phenotype remains unclear. This study focused on B cells in patients with NMOSD, hypothesizing that IL-6R Ab enables B cells to acquire regulatory functions by producing the anti-inflammatory cytokine IL-10. METHODS: Peripheral blood mononuclear cells were stimulated in vitro to induce the expansion of B-cell subsets, double-negative B cells (DNs; CD19+ IgD-, CD27-) and plasmablasts (PBs; CD19+, CD27hi, CD38hi). Whole B cells, DNs, or PBs were isolated after culture with IL-6R Ab, and IL-10 expression was quantified using quantitative PCR and a cytometric bead array. RNA sequencing was performed to identify the marker of regulatory PBs induced by IL-6R Ab. RESULTS: DNs and PBs were observed to expand in patients with NMSOD during the acute attacks. In the in vitro model, IL-6R Ab increased IL-10 expression in B cells. Notably, IL-10 expression increased in PBs but not in DNs. Using RNA sequencing, CD200 was identified as a marker of regulatory PBs among the differentially expressed upregulated genes. CD200+ PBs produced more IL-10 than CD200- PBs. Furthermore, patients with NMOSD who received satralizumab had a higher proportion of CD200+ PBs than patients during the acute attacks. DISCUSSION: Treatment with IL-6 signaling blockade elicited a regulatory phenotype in B cells and PBs. CD200+ PBs may be a marker of treatment responsiveness in the context of NMOSD pathophysiology.

  Lead, Jul. 2024, Neurology(R) neuroimmunology & neuroinflammation, 11(4) (4), e200266, English, International magazine

  [Refereed]

  Scientific journal

  Link to Kobe Univ. Repository (Kernel)


• Efficacy and safety of mycophenolate mofetil for steroid reduction in neuromyelitis optica spectrum disorder: a prospective cohort study.

  Ritsu Akatani, Norio Chihara, Shusuke Koto, Sotaro Mori, Takuji Kurimoto, Makoto Nakamura, Hisatsugu Tachibana, Yoshihisa Otsuka, Takehiro Ueda, Takashi Omori, Kenji Sekiguchi, Riki Matsumoto

  Neuromyelitis optica spectrum disorder (NMOSD) is a rare autoimmune inflammatory disease that can affect multiple generations and cause complications with long-term prednisolone treatment. This study aimed to evaluate the efficacy and safety of mycophenolate mofetil (MMF) in preventing NMOSD relapse while reducing prednisolone dosage. The trial involved nine patients with NMOSD who received MMF along with prednisolone dose reduction. MMF was effective in achieving prednisolone dose reduction without relapse in 77.8% of patients, with a significant decrease in mean annualized relapse rate. All adverse events were mild. The findings suggest that MMF could be a viable treatment option for middle-aged and older patients who require steroid reduction.Clinical trial registration number: jRCT, jRCTs051180080. Registered February 27th, 2019-retrospectively registered, https://jrct.niph.go.jp/en-latest-detail/jRCTs051180080.

  Lead, Jun. 2024, Immunological medicine, 47(2) (2), 85 - 92, English, International magazine

  [Refereed]

  Scientific journal

  Link to Kobe Univ. Repository (Kernel)


• Transcription Factor c-Maf Promotes Immunoregulation of Programmed Cell Death 1-Expressed CD8+ T Cells in Multiple Sclerosis.

  Shusuke Koto, Norio Chihara, Ritsu Akatani, Hiroko Nakano, Atsushi Hara, Kenji Sekiguchi, Riki Matsumoto, Tatsushi Toda

  BACKGROUND AND OBJECTIVES: Multiple sclerosis (MS) is an inflammatory demyelinating disease of the CNS. CD8+ T cells are prominently found at inflammatory sites. Recent advances in understanding checkpoint molecules, including programmed cell death 1 (PD-1), expressed on CD8+ T cells, highlight the immune regulatory roles of this T-cell subset; however, the role of CD8+ T cells in MS is unclear. Thus, we aimed to reveal the characteristics of PD-1-expressed (PD-1+) CD8+ T cells in MS. METHODS: We performed a cohort, case-control study for phenotyping analysis of PD-1+CD8+ T cells in disease remission and flare states using CSF and peripheral blood samples of 45 patients with MS or clinically isolated syndrome and 12 healthy subjects. We further analyzed the transcriptome of sorted PD-1+CD8+ T cells obtained from interferon (IFN)-β-treated patients and validated their regulatory machinery using in vitro cell culture assays with lentiviral gene transfer. RESULTS: In the disease remission state, PD-1+CD8+ T cells were decreased in the peripheral blood of patients with MS and resolved in patients treated with IFN-β treatment who showed immune regulatory cytokine interleukin (IL)-10 expression. In the disease flare state, we found that PD-1+CD8+ T cells were enriched in the CSF, which predicted a good response to subsequent IV steroid therapy. Transcriptome analysis of sorted PD-1+CD8+ T cells revealed the transcription factor c-Maf as a potential major regulator of the gene module, including multiple coinhibitory molecules. Furthermore, c-Maf expressed in CD8+ T cells induced PD-1 expression and production of IL-10 as well as suppressed alloactivated CD4+ T-cell survival. DISCUSSION: This study uncovered a favorable role of PD-1+CD8+ T cells against MS and demonstrated that c-Maf-driven IL-10 is an immune regulatory machinery.

  Jul. 2022, Neurology(R) neuroimmunology & neuroinflammation, 9(4) (4), English, International magazine

  [Refereed]

  Scientific journal


• Circulating plasmablasts and follicular helper T-cell subsets are associated with antibody-positive autoimmune epilepsy.

  Atsushi Hara, Norio Chihara, Ritsu Akatani, Ryusei Nishigori, Asato Tsuji, Hajime Yoshimura, Michi Kawamoto, Yoshihisa Otsuka, Yasufumi Kageyama, Takayuki Kondo, Frank Leypoldt, Klaus-Peter Wandinger, Riki Matsumoto

  Autoimmune epilepsy (AE) is an inflammatory disease of the central nervous system with symptoms that have seizures that are refractory to antiepileptic drugs. Since the diagnosis of AE tends to rely on a limited number of anti-neuronal antibody tests, a more comprehensive analysis of the immune background could achieve better diagnostic accuracy. This study aimed to compare the characteristics of anti-neuronal antibody-positive autoimmune epilepsy (AE/Ab(+)) and antibody-negative suspected autoimmune epilepsy (AE/Ab(-)) groups. A total of 23 patients who met the diagnostic criteria for autoimmune encephalitis with seizures and 11 healthy controls (HC) were enrolled. All patients were comprehensively analyzed for anti-neuronal antibodies; 13 patients were identified in the AE/Ab(+) group and 10 in the AE/Ab(-) group. Differences in clinical characteristics, including laboratory and imaging findings, were evaluated between the groups. In addition, the immunophenotype of peripheral blood mononuclear cells (PBMCs) and CSF mononuclear cells, particularly B cells and circulating Tfh (cTfh) subsets, and multiplex assays of serum and CSF were analyzed using flow cytometry. Patients with AE/Ab(+) did not show any differences in clinical parameters compared to patients with AE/Ab(-). However, the frequency of plasmablasts within PBMCs and CSF in patients with AE/Ab(+) was higher than that in patients with AE/Ab(-) and HC, and the frequency of cTfh17 cells and inducible T-cell co-stimulator (ICOS) expressing cTfh17 cells within cTfh subsets was higher than that in patients with AE/Ab(-). Furthermore, the frequency of ICOShighcTfh17 cells was positively correlated with that of the unswitched memory B cells. We also found that IL-12, IL-23, IL-6, IL-17A, and IFN-γ levels were elevated in the serum and IL-17A and IL-6 levels were elevated in the CSF of patients with AE/Ab(+). Our findings indicate that patients with AE/Ab(+) showed increased differentiation of B cells and cTfh subsets associated with antibody production. The elevated frequency of plasmablasts and ICOS expressing cTfh17 shift in PBMCs may be indicative of the presence of antibodies in patients with AE.

  2022, Frontiers in immunology, 13, 1048428 - 1048428, English, International magazine

  [Refereed]

  Scientific journal


• 多発性硬化症の病態評価における光干渉断層計(OCT)の意義についての検討

  赤谷 律, 千原 典夫, 古東 秀介, 盛 崇太朗, 栗本 拓治, 立花 久嗣, 大塚 喜久, 上田 健博, 関口 兼司

  (一社)日本神経学会, Nov. 2019, 臨床神経学, 59(Suppl.) (Suppl.), S309 - S309, Japanese


• Validation of the Guy's Neurological Disability Scale as a screening tool for cognitive impairment in multiple sclerosis.

  Ritsu Akatani, Norio Chihara, Hisatsugu Tachibana, Shusuke Koto, Hisatomo Kowa, Fumio Kanda, Riki Matsumoto, Tatsushi Toda

  OBJECTIVES: Cognitive impairment is a common symptom affecting daily activities of the patients with multiple sclerosis (MS). Various cognitive evaluation tests are available, yet most of them are complex and time-consuming to perform in outpatient clinics. In this study, we aimed to validate a Japanese version of the Guy's Neurological Disability Scale (GNDS) as a user-friendly tool to evaluate comprehensive disabilities in MS including cognitive function. METHODS: Questions of the GNDS were translated into Japanese and named GNDS-J. Forty-four patients were examined by the Expanded Disability Status Scale (EDSS), the Paced Auditory Serial Addition Test (PASAT), the Symbol Digit Modalities Test (SDMT), the vitality scale, and the GNDS-J in the same time at remission state. RESULTS: The GNDS-J scores correlated with the EDSS scores(r = 0.61), and inversely correlated with the PASAT2/1(r=-0.56/-0.49) scores and the SDMT scores (r=-0.68), whereas the GNDS-J did not show any correlation with the vitality scale. Furthermore, eleven patients were evaluated over 5 years for changes in these scores. Eight out of 11 patients had exacerbated GNDS, and all of these patients experienced clinical relapse during this period. CONCLUSION: The GNDS-J is a valid tool to perform in outpatient clinics, which could provide a comprehensive scale for evaluating symptoms of MS, thus the disease activity by repeated measure.

  Lead, Oct. 2019, Multiple sclerosis and related disorders, 35, 272 - 275, English, International magazine

  [Refereed]

  Scientific journal


• [Increased disease activity in a case of multiple sclerosis after switching treatment from fingolimod to natalizumab].

  Ritsu Akatani, Norio Chihara, Kimitaka Katanazaka, Takehiro Ueda, Kenji Sekiguchi, Riki Matsumoto

  A 42-year-old woman diagnosed with multiple sclerosis (MS) at the age of 37 was initially treated with interferon-β IM. The frequency of clinical relapses was twice in 4 years. At the age of 41, due to difficulty in administering muscle injections, an oral medication fingolimod was started. However, it was discontinued after a month due to decreased lymphocyte count, following which natalizumab was administered. The number of relapses increased 3 times in eleven months, and the number of T2 lesions on the MRI increased from 12 to 23. Natalizumab was discontinued because the test for the anti-natalizumab antibody was positive. It was suspected that both, the rebound syndrome caused by fingolimod cessation and the drug neutralization by anti-natalizumab antibodies, were associated with the exacerbation of disease activity. Thus, careful attention should be paid to potential occurrence of these events post switching between disease-modifying drugs for treating MS with high activity.

  Lead, Aug. 2019, Rinsho shinkeigaku = Clinical neurology, 59(8) (8), 536 - 540, Japanese, Domestic magazine

  [Refereed]

  Scientific journal


• フィンゴリモドからナタリズマブへ疾患修飾薬変更後に疾患活動性が上昇した多発性硬化症の1例

  赤谷 律, 千原 典夫, 刀坂 公崇, 上田 健博, 関口 兼司, 松本 理器

  (一社)日本神経学会, Aug. 2019, 臨床神経学, 59(8) (8), 536 - 540, Japanese


• 疾患修飾薬変更後に再発を繰り返し、抗ナタリズマブ抗体が陽性であった多発性硬化症の1例

  赤谷 律, 千原 典夫, 刀坂 公崇, 立花 久嗣, 大塚 喜久, 上田 健博, 関口 兼司

  (一社)日本神経治療学会, Nov. 2018, 神経治療学, 35(6) (6), S220 - S220, Japanese


• 緩徐に進行し、遺伝性との鑑別を要した孤発性クロイツフェルト・ヤコブ病の1例

  刀坂 公崇, 赤谷 律, 大塚 喜久, 高田 真利子, 千原 典夫, 上田 健博, 関口 兼司

  (一社)日本神経学会, Sep. 2018, 臨床神経学, 58(9) (9), 585 - 585, Japanese


• 抗ナタリズマブ抗体が陽性となった多発性硬化症の1例

  赤谷 律, 千原 典夫, 刀坂 公崇, 立花 久嗣, 大塚 喜久, 上田 健博, 関口 兼司, 古和 久朋, 戸田 達史

  (一社)日本神経免疫学会, Sep. 2018, 神経免疫学, 23(1) (1), 142 - 142, Japanese


• Guy's Neurological Disability Scaleを用いた多発性硬化症の非身体障害機能評価

  赤谷 律, 千原 典夫, 立花 久嗣, 古東 秀介, 大塚 喜久, 上田 健博, 関口 兼司, 古和 久朋, 戸田 達史

  (一社)日本神経免疫学会, Oct. 2017, 神経免疫学, 22(1) (1), 135 - 135, Japanese


• パーキンソニズムを呈した22q11.2欠失症候群の1例

  赤谷 律, Fukuoka Hidenori, 本岡 里英子, 千原 典夫, 佐竹 渉, 関口 兼司, 濱口 浩敏, 古和 久朋, Kanda Fumio, 戸田 達史

  (一社)日本神経学会, Jan. 2014, 臨床神経学, 54(1) (1), 65 - 65, Japanese

  Research society

• 脳脊髄液の免疫細胞と視神経脊髄炎スペクトラム障害

  赤谷 律, 千原典夫

  Lead, Oct. 2025, 実験医学 2025年11月号, 43(18) (18)


• Induction of immune rebalancing with anti-IL-6R antibody treatment in patients with NMOSD

  Norio Chihara, Ritsu Akatani, Ryosuke Takeda, Yuka Tagawa, Kyoka Shiroma, Asato Tsuji, Shota Nishii, Kimitaka Katanazaka, Kento Matoba, Shusuke Koto, Masayuki Taniguchi, Tomoyuki Furuyashiki, Kenji Sekiguchi

  Sep. 2025, MULTIPLE SCLEROSIS JOURNAL, 31(3) (3), 465 - 465, English

  Summary international conference


• 多発性硬化症患者CD8+T細胞PD-1発現と再発時治療反応性や長期予後との関係

  古東秀介, 千原典夫, 武田涼輔, 西居正汰, 辻麻人, 刀坂公崇, 末廣大知, 的場健人, 尾谷真弓, 赤谷律, 関口兼司

  2025, 日本神経学会学術大会プログラム・抄録集, 66th


• 認知機能障害が遷延した自己免疫性GFAPアストロサイトパチー2症例の異なる治療経過

  福田まり, 福田まり, 千原典夫, 都留朝希, 都留朝希, 田中智子, 尾谷真弓, 赤谷律, 的場健人, 古東秀介, 木村暁夫, 下畑享良, 関口兼司, 松本理器

  2025, 日本神経学会学術大会プログラム・抄録集, 66th


• 視神経脊髄炎スペクトラム障害・多発性硬化症とB細胞

  赤谷 律, 千原典夫

  Lead, Jan. 2025, 炎症と免疫, 33(1) (1), Japanese

  Introduction scientific journal


• 多発性硬化症患者脳脊髄液のCD8+ T細胞上のPD-1発現上昇が良好な長期予後と相関する

  古東 秀介, 千原 典夫, 城間 京香, 辻 麻人, 刀坂 公崇, 西居 正汰, 的場 健人, 赤谷 律, 十河 正弥, 関口 兼司, 松本 理器

  (一社)日本神経学会, Oct. 2024, 臨床神経学, 64(Suppl.) (Suppl.), S236 - S236, Japanese


• IL-6 Blockade in NMOSD: Unveiling B Cell Dynamics and Regulatory Plasmablast Induction

  Ritsu Akatani, Norio Chihara, Atsushi Hara, Asato Tsuji, Shusuke Koto, Riki Matsumoto

  Sep. 2024, MULTIPLE SCLEROSIS JOURNAL, 30(3) (3), 1005 - 1005, English

  Summary international conference


• 視神経脊髄炎(NMOSD)における重症化指標としてのリンパ球分画評価の妥当性

  城間京香, 千原典夫, 辻麻人, 武田涼輔, 原敦, 原敦, 赤谷律, 古東秀介, 松本理器

  2024, 日本臨床免疫学会総会プログラム・抄録集, 52nd


• PD-1 positive CD8+T cells are associated with better clinical outcomes in patients with the early stage of multiple sclerosis

  Norio Chihara, Shusuke Koto, Ritsu Akatani, Asato Tsuji, Kimitaka Katanazaka, Shota Nishii, Ryosuke Takeda, Kyoka Shiroma, Kenji Sekiguchi, Riki Matsumoto

  Oct. 2023, MULTIPLE SCLEROSIS JOURNAL, 29, 814 - 815, English

  Summary international conference


• 多発性硬化症患者脳脊髄液におけるCD8+T細胞上のPD-1発現上昇が良好な長期予後の指標となりうる

  古東 秀介, 千原 典夫, 赤谷 律, 辻 麻人, 刀坂 公崇, 西居 正汰, 的場 健人, 十河 正弥, 関口 兼司, 松本 理器

  (一社)日本神経免疫学会, Sep. 2023, 神経免疫学, 28(1) (1), 185 - 185, Japanese


• 日本人MSにおける神経障害進行指標としてのSDMTの有用性の検証

  城間 京香, 千原 典夫, 赤谷 律, 古東 秀介, 的場 健人, 十河 正弥, 関口 兼司, 松本 理器

  (一社)日本神経免疫学会, Sep. 2023, 神経免疫学, 28(1) (1), 207 - 207, Japanese


• 多発性硬化症患者脳脊髄液におけるCD8+T細胞上のPD-1発現上昇が良好な長期予後の指標となりうる

  古東 秀介, 千原 典夫, 赤谷 律, 辻 麻人, 刀坂 公崇, 西居 正汰, 的場 健人, 十河 正弥, 関口 兼司, 松本 理器

  (一社)日本神経免疫学会, Sep. 2023, 神経免疫学, 28(1) (1), 185 - 185, Japanese


• 日本人MSにおける神経障害進行指標としてのSDMTの有用性の検証

  城間 京香, 千原 典夫, 赤谷 律, 古東 秀介, 的場 健人, 十河 正弥, 関口 兼司, 松本 理器

  (一社)日本神経免疫学会, Sep. 2023, 神経免疫学, 28(1) (1), 207 - 207, Japanese


• 転写因子c-Mafは多発性硬化症におけるCD8+T細胞のPD-1発現を促進し,免疫制御機能を発揮する

  古東 秀介, 千原 典夫, 赤谷 律, 原 敦, 関口 兼司, 松本 理器, 戸田 達史

  (一社)日本神経免疫学会, Oct. 2022, 神経免疫学, 27(1) (1), 122 - 122, Japanese


• NMO2 視神経脊髄炎に対するミコフェノール酸モフェチルによる再発抑制と安全性評価のためのオープン試験

  赤谷 律, 千原 典夫, 古東 秀介, 大森 崇, 関口 兼司, 松本 理器

  (一社)日本神経免疫学会, Oct. 2022, 神経免疫学, 27(1) (1), 153 - 153, Japanese


• 異なる治療反応性を示した免疫チェックポイント阻害薬誘発筋炎の2症例

  原 敦, 千原 典夫, 赤谷 律, 山口 星一郎, 小牧 遼平, 末廣 大知, 森本 耕平, 野田 佳克, 関口 兼司, 松本 理器

  日本神経免疫学会, Oct. 2020, 神経免疫学, 25(1) (1), 174 - 174, Japanese


• 抗GQ1b抗体症候群

  赤谷 律, 千原典夫

  Lead, Feb. 2020, Monthly Book OCULISTA(オクリスタ), 83, Japanese

  Introduction scientific journal


• 多発性硬化症の急性期治療反応性と相関する脳脊髄液中のPD-1陽性CD8+ T細胞の役割

  古東 秀介, 千原 典夫, 赤谷 律, 関口 兼司, 戸田 達史

  (一社)日本神経学会, Nov. 2019, 臨床神経学, 59(Suppl.) (Suppl.), S277 - S277, Japanese


• NMOに対するMMFによる再発抑制と安全性確認のためのオープン試験

  千原 典夫, 古東 秀介, 赤谷 律, 立花 久嗣, 大塚 喜久, 上田 健博, 関口 兼司

  (一社)日本神経学会, Nov. 2019, 臨床神経学, 59(Suppl.) (Suppl.), S319 - S319, Japanese


• 多発性硬化症の急性期治療反応性と相関する脳脊髄液中のPD-1陽性CD8+ T細胞の役割

  古東 秀介, 千原 典夫, 赤谷 律, 関口 兼司, 戸田 達史

  (一社)日本神経学会, Nov. 2019, 臨床神経学, 59(Suppl.) (Suppl.), S277 - S277, Japanese

  [Refereed]

  Summary national conference


• PD-1陽性CD8+T細胞は多発性硬化症の治療効果を反映する

  古東 秀介, 千原 典夫, 赤谷 律, 関口 兼司, 戸田 達史

  (一社)日本神経学会, Dec. 2018, 臨床神経学, 58(Suppl.) (Suppl.), S217 - S217, Japanese

  [Refereed]


• 日本語版Guy's Neurological Disability Scaleを用いた多発性硬化症の臨床的評価

  赤谷 律, 千原 典夫, 渡部 俊介, 立花 久嗣, 古東 秀介, 大塚 喜久, 上田 健博, 関口 兼司, 古和 久朋, 戸田 達史

  (一社)日本神経学会, Dec. 2018, 臨床神経学, 58(Suppl.) (Suppl.), S268 - S268, Japanese

  [Refereed]


• 多発性硬化症におけるPD-1陽性CD8+T細胞の脳脊髄液および末梢血での比較

  古東 秀介, 千原 典夫, 赤谷 律, 関口 兼司, 戸田 達史

  日本神経免疫学会, Sep. 2018, 神経免疫学, 23(1) (1), 142 - 142, Japanese

  [Refereed]


• 抗ミトコンドリア抗体陽性筋炎におけるミトコンドリア機能障害についての検討

  上中 健, 古和 久朋, 赤谷 律, 遠藤 浩信, 井元 万紀子, 本岡 里英子, 立花 久嗣, 千原 典夫, 関 恒慶, 安井 直子, 久我 敦, 関口 兼司, 濱口 浩敏, Kanda Fumio, 戸田 達史

  (一社)日本神経学会, Dec. 2013, 臨床神経学, 53(12号) (12号), 1631 - 1631, Japanese

  Meeting report


• ヒトパピローマウイルスワクチン接種に伴う急性散在性脳脊髄炎が疑われた2症例の検討

  関口 兼司, 赤谷 律, 遠藤 浩信, 井元 万紀子, 上中 健, 本岡 里英子, 立花 久嗣, 千原 典夫, 鷲田 和夫, 安井 直子, 久我 敦, 濱口 浩敏, 古和 久朋, Kanda Fumio, 戸田 達史

  (一社)日本神経学会, Dec. 2013, 臨床神経学, 53(12号) (12号), 1472 - 1472, Japanese


• フィンゴリモド導入における初期脱落例の検討

  遠藤 浩信, 千原 典夫, 赤谷 律, 井元 万紀子, 上中 健, 本岡 里英子, 立花 久嗣, 安井 直子, 鷲田 和夫, 久我 敦, 関口 兼司, 濱口 浩敏, 古和 久朋, Kanda Fumio, 戸田 達史

  (一社)日本神経学会, Dec. 2013, 臨床神経学, 53(12号) (12号), 1625 - 1625, Japanese

  Meeting report

• 眼疾患アトラスシリーズ 第5巻 眼と全身病アトラス

  赤谷 律, 千原典夫

  Joint work, 抗GQ1b抗体症候群, 総合医学社, May 2021

• 免疫性神経疾患における病態保護的B細胞誘導療法の開発

  赤谷 律

  日本学術振興会, 科学研究費助成事業, 若手研究, 神戸大学, 01 Apr. 2023 - 31 Mar. 2026


• 視神経脊髄炎スペクトラム障害におけるB細胞制御機構の解明

  赤谷 律

  日本学術振興会, 科学研究費助成事業, 研究活動スタート支援, 神戸大学, 30 Aug. 2021 - 31 Mar. 2023

  本研究では、以下の3つの方法を用いて研究を実施する計画とした。それぞれの計画についての実績は下記のとおりである。 ①in vitro培養系を用いて病原性ないし制御性B細胞分化誘導条件を検討する計画については、予備実験でB細胞のPBへの分化誘導系を確立し、抗IL-6受容体抗体の添加によりPBにおける制御性B細胞が誘導できることを確認した。また、RNAシークエンスによる網羅的遺伝子発現解析を行い、免疫制御性の機能を発揮するプラズマブラストのマーカー候補として、CD200分子が浮上し、現在タンパクレベルでのこの分子の機能を検証している。 ②アストロサイトとの共培養系を用いてNMOSDにおける中枢神経内のB細胞動態を明らかにする計画については、予備実験としてB細胞とアストロサイトとの共培養系を用いることでアストロサイトがPBの生存を延長することを確認し、アストロサイトとの共培養によってPBのIL-10発現が上昇することが見出せたが、IL-6シグナルの阻害による有意な変化はみられなかった。また、この共培養の系ではB細胞の数が著減する場合があり中枢神経内での病態を明確に反映した所見と言えるかどうかは未だはっきりしていない。 ③in vivoモデルを用いた制御性B細胞誘導の鍵となる分子を検証する計画については、最終段階として実験的自己免疫性脳脊髄炎（EAE）マウスモデルを用いて候補分子発現細胞の移入実験による機能解析を行い、加えて候補分子のノックアウトマウスを作成しEAEモデルを用いた実証実験に向けた準備を行う予定であるが、未だ実現には至っていない。