研究者詳細 - 一宮　慎吾

アトピー性皮膚炎は本邦の小児の約1割が罹患し，罹患者の生活の質を著しく低下させる．さらにアトピー性皮膚炎自体が気管支喘息やアレルギー性結膜炎など種々の慢性アレルギー疾患の根底にある可能性が分子免疫学的にも支持されつつあり，その病態の機序の解明が急がれている．近年，アトピー性皮膚炎の患部のケラチノサイトがthymic stromal lymphopoietin（TSLP）を高産生することが明らかとなった．TSLPはTSLP受容体（TSLPR）を発現する樹状細胞を介してTh0細胞をTh2細胞へと分化させることで，アトピー・アレルギー疾患の病態形成に中心的役割を果たすと考えられている．我々は今回，表皮ケラチノサイトにおけるTSLPRの発現を明らかとした．また，表皮ケラチノサイト初代培養細胞および表皮モデルHaCaT細胞を用いた検討において，TSLPRの発現は表皮幹細胞因子p63を介した自然免疫経路によって制御されていた．興味深いことに表皮に対するTSLP刺激は更なるTSLP産生を惹起し，その他の炎症性サイトカインの発現も促進していた．これらの結果からTSLPはオートクラインあるいはパラクラインによってケラチノサイト自身にも作用するループを形成し，アトピー性皮膚炎患部表皮の炎症環境の形成，維持に関与していると考えられる．

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O58-3 アトピー型気管支喘息患者における血清IL-9の検討(サイトカイン・ケモカイン1,口演,第62回日本アレルギー学会秋季学術大会)

重原克則, 伊藤進, 井上祐二, 一宮慎吾

アレルギー ( 一般社団法人日本アレルギー学会 ) 61 ( 9-10 ) 1541 2012年

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症例解説-リンパ節マントル細胞リンパ腫の病理組織診断

一宮慎吾

病理と臨床 27 1094 - 1095 2009年

JNK特異的阻害剤による免疫抑制の可能性とその機序

宮島正博, 森川雅之, 田畑哲寿, 一宮慎吾, 佐藤昇志, 安倍十三夫

日本外科学会雑誌 ( 一般社団法人日本外科学会 ) 107 ( 2 ) 709 - 709 2006年03月

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Clinical significance of vascular endothelial growth factor-C and vascular endothelial growth factor receptor 3 in patients with T1 lung adenocarcinoma

H Kojima, N Shijubo, G Yamada, S Ichimiya, S Abe, M Satoh, N Sato

CANCER ( JOHN WILEY & SONS INC ) 104 ( 8 ) 1668 - 1677 2005年10月

BACKGROUND. Vascular endothelial growth factor-C (VEGF-C) plays an important role in lymphangiogenesis and activates VEGF receptor-3 (VEGFR-3). Lymphatic spread is an important prognostic factor in patients with lung adenocarcinoma. The aim of the current study was to determine whether the expression of VEGF-C and VEGFR-3 correlates with clinicopathologic factors and prognosis in patients with TNM classification T1 lung adenocarcinoma. METHODS. The authors conducted a retrospective review of 129 consecutive patients who underwent complete resection for T1 lung adenocarcinoma. Immuno- histochernical staining for VEGF-C, VEGF, VEGFR-3, CD34 (microvessels), tryptase (mast cells), and CD68 (macrophages) was performed to statistically analyze clin- icopathologic implications of VEGF-C and VEGFR-3 status. RESULTS. Of 129 patients with T1 lung adenocarcinoma, 56 (43.3%) patients were positive for tumor-cell VEGF-C and 73 (56.6%) and 69 (53.5%) patients were positive for tumor-cell and endothelial-cell VEGFR-3, respectively. Patients with positive staining for tumor-cell VEGF-C showed significantly less favorable survival rates than patients with negative staining (P = 0.031). The survival rates of patients with positive staining for tumor-cell and endothelial-cell VEGFR-3 were significantly cantly lower than those with negative staining (P = 0.0034 and P = 0.0020, respectively). Patients with positive staining for both tumor-cell VEGF-C and endothelial-cell VEGFR-3 exhibited the most unfavorable prognoses. Multivariate analysis demonstrated that coexpression of tumor-cell VEGF-C and endothelialcell VEGFR-3 was an independent negative prognostic factor (P = 0.0129) as well as N factor (P = 0.0020). CONCLUSIONS. VEGF-C and VEGFR-3 status may be indicative of survival rates for patients with T1 lung adenocarcinoma.

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重症筋無力症の胸腺におけるCHRNA9遺伝子の発現(縦隔腫瘍 (3), 第22回日本呼吸器外科学会総会)

小柳哲也, 渡辺敦, 馬渡徹, 安倍十三夫, 一宮慎吾

日本呼吸器外科学会雑誌 ( 特定非営利活動法人日本呼吸器外科学会 ) 19 ( 3 ) 374 - 374 2005年05月

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HLA-DR- and CD11c-positive dendritic cells penetrate beyond well-developed epithelial tight junctions in human nasal mucosa of allergic rhinitis

K Takano, T Kojima, M Go, M Murata, S Ichimiya, T Himi, N Sawada

JOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY ( HISTOCHEMICAL SOC INC ) 53 ( 5 ) 611 - 619 2005年05月

The epithelial barrier of the upper respiratory tract plays a crucial role in host defense. In this study, to elucidate whether there is antigen monitoring by dendritic cells (DCs) beyond the epithelial tight-junction barrier in allergic rhinitis, we investigated the expression and function of tight junctions and characterized DCs in the epithelium of nasal mucosa from patients with allergic rhinitis. In reverse transcription-polymerase chain reaction, mRNAs of tight-junction proteins occludin, JAM-1, ZO-1, and claudin-1, -4, -7, -8, -12, -13, and -14 were detected in the nasal mucosa. Occludin, JAM-1, and ZO-1 were colocalized in the uppermost layer in the pseudostratified epithelium of the nasal mucosa, whereas claudin-1, -4, and -7 were found throughout the epithelium. in freeze-fracture replicas of the nasal mucosa, continuous tight-junction strands formed well-developed networks. Epithelial barrier function measured by a dye tracer was well maintained in occludin-positive tight junctions in the epithelium of the nasal mucosa. HLA-DR- and CD11c-positive DCs expressed claudin-1 and penetrated beyond occludin in the epithelium of the nasal mucosa with, but not without, allergic rhinitis. These results indicate that DCs may easily access antigens beyond epithelial tight junctions in the human nasal mucosa of allergic rhinitis.

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Effects of inhaled FK 506 on the suppression of acute rejection after lung transplantation: Use of a rat orthotopic lung transplantation model

A Ingu, K Komatsu, S Ichimiya, N Sato, Y Hirayama, M Morikawa, T Abe

JOURNAL OF HEART AND LUNG TRANSPLANTATION ( ELSEVIER SCIENCE INC ) 24 ( 5 ) 538 - 543 2005年05月

Background: FK 506 inhalant was recently developed for localized administration. We investigated its effects on acute lung allograft rejection and compared its efficacy with that of intramuscular administration of FK 506. Methods: Rats (n = 123) with orthotopic left lung transplantation were divided into 9 groups. Six groups inhaled FK 506 (5 puffs, 10 puffs or 20 puffs per day), or were given intramuscular administration of FK 506 (0.05, 0.1 or 1.0 mg/kg/day). The other groups included rats receiving an isograft, rats with an untreated allograft, and a placebo group. All groups (n = 6 each) were monitored for 14 days post-operatively as an end-point and graft survival time was determined. The remaining animals were killed 4 days after transplantation. The histologic grade of rejection was determined for all groups (n = 6 each). With both (n = 3 each) inhalation therapy and intramuscular administration of FK 506, which showed similar degrees of effectiveness, both blood FK 506 concentration and cytokine expression in the graft and spleen were evaluated. Results: FK 506 inhalation therapy extended allograft survival time and reduced histologic rejection on Day 4 in all groups. Graft survival time and histologic rejection scores at a dose of 10 puffs/day were comparable to those with 0.1 mg/kg/day of intramuscular FK 506. Trough concentrations of FK 506 in blood were detectable with 0.1 mg/kg/day of intramuscular FK 506, but not with 10 puffs/day. The messenger RNA expression levels of interferon-gamma in the lung allograft was suppressed significantly at a dose of 10 puffs/day. Conclusions: FK 506 inhalant enhances acute lung allograft survival with lower blood concentrations than when using comparable intramuscular administration. J Heart Lung Transplant 2005;24:538-43. Copyright (c) 2005 by the International Society for Heart and Lung Transplantation.

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A calcium binding protein, S100A4, mediates T cell dependent cytotoxicity as a transformation-associated antigen

N Kondo, S Ichimiya, Y Tamura, A Tonooka, S Koshiba, T Torigoe, K Kamiguchi, K Takenaga, N Sato

MICROBIOLOGY AND IMMUNOLOGY ( CENTER ACADEMIC PUBL JAPAN ) 49 ( 1 ) 49 - 56 2005年

The nature of the target molecule of TCRgammadelta T cell-mediated lysis remains to be determined. As we previously reported, #067 monoclonal antibody (mAb) recognizes one of the transformation-associated antigens, designated as #067 antigen. This antigen is expressed on the cell surface of rat fibrosarcoma W31 cells, which are established by transformation of fetal fibroblastic WFB cells with H-ras oncogene. It has been suggested that the #067 antigen is a target molecule for TCRgammadelta T cells since #067 mAb inhibited TCRgammadelta T cell-mediated lysis against #067 positive cells. In this study we attempted to identify the protein sequence of the #067 antigen. By using molecular cloning techniques, we demonstrated that a calcium binding protein, S100A4, was possibly one and the same molecule as the #067 antigen. It was shown that the expression of S100A4 was higher in W31 cells than in WFB cells at transcription and protein level. Flow cytometry and immunocytochemical studies showed that #067 antigen partially co-localized with S100A4 on the cell surface as well as the cytoplasm of W31 cells. Moreover. rabbit anti-S100A4 polyclonal antibodies (pAb) inhibited TCRgammadelta T cell-mediated lysis against #067 positive cells. Our results indicated that S100A4 may play a role as a possible target molecule for TCRgammadelta T cell-mediated lysis although how S100A4 is involved in TCRgammadelta T cell-mediated lysis remains to be determined.

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Expression and function of tight junctions in the crypt epithelium of human palatine tonsils

M Go, T Kojima, K Takano, M Murata, S Ichimiya, H Tsubota, T Himi, N Sawada

JOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY ( HISTOCHEMICAL SOC INC ) 52 ( 12 ) 1627 - 1638 2004年12月

The human palatine tonsils have surface and crypt stratified epithelium and may be initiated via the epithelium to mount immune responses to various presenting antigens. Here we investigated the expression and function of tight junctions in the epithelium of human palatine tonsils from patients with tonsillar hypertrophy or recurrent tonsillitis. Occludin, ZO-1, JAM-1, and claudin-1, -3, -4, -7, -8, and -14 mRNAs were detected in tonsillar hypertrophy. Occludin and claudin-14 were expressed in the uppermost layer of the tonsil surface epithelium, whereas ZO-1, JAM-1, and claudin-1, -4, and -7 were found throughout the epithelium. In the crypt epithelium, claudin-4 was preferentially expressed in the upper layers. In freeze-fracture replicas, short fragments of continuous tight junction strands were observed but never formed networks. In the crypt epithelium of recurrent tonsillitis, the tracer was leaked from the surface regions where occludin and claudin-4 disappeared. Occludin, ZO-1, JAM-1, and claudin-1, -3, -4, and -14, but not claudin-7, mRNAs were decreased in recurrent tonsillitis compared with those of tonsillar hypertrophy. These studies suggest unique expression of tight junctions in human palatine tonsillar epithelium, and the crypt epithelium may possess an epithelial barrier different from that of the surface epithelium.

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