研究者詳細 - 一宮　慎吾

Misc - 一宮　慎吾

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Crisscross CTL induction by SYT-SSX junction peptide and its HLA-A*2402 anchor substitute

K Ida, S Kawaguchi, Y Sato, T Tsukahara, Y Nabeta, H Sahara, H Ikeda, T Torigoe, S Ichimiya, K Kamiguchi, T Wada, S Nagoya, H Hiraga, A Kawai, T Ishii, N Araki, A Myoui, S Matsumoto, T Ozaki, H Yoshikawa, T Yamashita, N Sato

JOURNAL OF IMMUNOLOGY ( AMER ASSOC IMMUNOLOGISTS ) 173 ( 2 ) 1436 - 1443 2004年07月

To investigate the effects of anchor substitutions in SYT-SSX junction peptide, an HLA-A24 anchor residue (position 9) of the SYT-SSX B peptide (GYDQIMPKK) was substituted to more favorable residues according to the HLA-A24-binding motif. Among four substitutes constructed, a substitute with isoleucine (termed K9I peptide) most apparently enhanced the affinity for HLA-A24 molecule. Subsequent in vitro CTL induction analysis using PBMCs of 15 HLA-A24(+) synovial sarcoma patients revealed that the original B peptide allowed to induce synovial sarcoma-specific CTLs from 7 patients (47%), whereas such CTLs were inducible from 12 patients (80%) with K9I peptide. Moreover, the extent of cytotoxicity against HLA-A24(+) synovial sarcoma cell lines was higher in K9I peptide-induced CTLs than B peptide-induced CTLs. Influence of anchor substitution on peptide/TCR interaction was evaluated by cytotoxicity assays against autologous cells and tetramer analysis., CTLs induced from a synovial sarcoma patient using K9I peptide did not lyse autologous PHA blasts or EBV-infected B cells. In vitro stimulations of PBMCs from 5 HLA-A24(+) synovial sarcoma patients with K9I peptide increased the frequency of T cells reacting with both HLA-A24/K9I peptide tetramer and HLA-A24/B peptide tetramer. In-contrast, the frequency of T cells reacting with HLA/HIV-derived peptide tetramer remained low. These findings support the validity in design of anchor residue substitution in SYT-SSX fusion gene-derived peptide, and provide a potential clue to the current stagnation in vaccination trials of fusion gene-derived natural junction peptides.

DOI

Expression profiles and functional implications of p53-like transcription factors in thymic epithelial cell subtypes

T Kikuchi, S Ichimiya, T Kojima, L Crisa, S Koshiba, A Tonooka, N Kondo, PT van der Saag, S Yokoyama, N Sato

INTERNATIONAL IMMUNOLOGY ( OXFORD UNIV PRESS ) 16 ( 6 ) 831 - 841 2004年06月

In this study, we investigated the localization and functional significance of p53 tumor suppressor-like molecules, p63 and p73, in human thymic epithelial cells (TECs). Immunohistochemical studies showed particular distribution profiles of p63 and p73 in thymic epithelium, in which cortical TECs preferentially expressed p63 in their nuclei whereas subcapsular and medullary TECs expressed both p63 and p73 in their nuclei. The wide distribution of p63 in TECs was further suggested by studies using TECs of primary culture. In vitro studies using two human TEC lines demonstrated that p63 was capable of up-regulating intercellular adhesion molecule-1 (ICAM-1) and enhancing the production of IL-6 and IL-8. Moreover, in vitro studies also indicated that p73, but not p63, had the capacity to induce granulocyte macrophage colony stimulating factor (GM-CSF) and granulocyte colony stimulating factor (G-CSF) in the TEC lines. These findings suggest that p63 would regulate the cell adhesive property through ICAM-1/LFA-1 interaction and the production of IL-6 and IL-8, probably in all TEC subtypes. p73 in subcapslar and medullary TECs was suggested to play a role in the regulation of the production of GM-CSF and G-CSF, which might stimulate other stromal cells such as dendritic cells, macrophages and endothelial cells around these regions.

DOI PubMed CiNii

Tumor-derived heat shock protein 70-pulsed dendritic cells elicit tumor-specific cytotoxic T lymphocytes (CTLs) and tumor immunity

G Ueda, Y Tamura, Hirai, I, K Kamiguchi, S Ichimiya, T Torigoe, H Hiratsuka, H Sunakawa, N Sato

CANCER SCIENCE ( JAPANESE CANCER ASSOC ) 95 ( 3 ) 248 - 253 2004年03月

Vaccination with autologous tumor-derived heat shock proteins (Hsp), such as Hsp70, Hsp90 and gp96, has been demonstrated to elicit specific immune responses against the tumor from which the Hsps were isolated. The effect of Hsp immunization is wholly dependent on the presence of functional antigen-presenting cells (APCs) in the immunized host, and Hsp receptors on APCs have recently been identified. Here we show that bone marrow-derived dendritic cells (DCs) are able to internalize HSP-peptide complex and that peptides are re-presented by DCs via the major histocompatibility complex (MHC) class I presentation pathway. In addition, immunization with tumor-derived HSP-pulsed IDCs induces strong cytotoxic T cell (CTL) responses against multiple antigenic peptides in a transporter-associated antigen processing (TAP)-dependent manner. The results of the present study provide strong evidence of an efficient cross-priming activity of Hsp70, which could be exploited in the development of new and more effective immunotherapeutic strategies for cancer patients.

DOI PubMed CiNii

Polymorphism of Clara cell 10-kD protein gene of sarcoidosis

T Ohchi, N Shijubo, Kawabata, I, S Ichimiya, S Inomata, A Yamaguchi, Y Umemori, Y Itoh, S Abe, Y Hiraga, N Sato

AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE ( AMER THORACIC SOC ) 169 ( 2 ) 180 - 186 2004年01月

Clara cell 10-kD protein (CC10) exhibits potent antiinflammatory properties. G38A polymorphism was found in the CC10 gene. We investigated the genetic influence of the allele on the development of sarcoiclosis using case control analysis in a Japanese population (265 sarcoiclosis cases and 258 control subjects). The A allele frequency in sarcoiclosis cases (45.1%) was significantly higher than healthy control subjects (34.9%, p = 0.0002). According to outcomes, we divided 223 patients with follow-up periods of 3 years or more into two subgroups (55 progressive and 168 regressive disease). The A allele frequency in patients with progressive disease was significantly higher than control subjects (odds ratio = 4.55; 95% confidence interval, 2.97-6.97; p < 0.0001), whereas that of regressive disease was not. The A/A genotypes had significantly lower bronchoalveolar lavage fluid CC10 levels than the G/G (nonsmokers, p = 0.0054, and smokers, p = 0.0045) and G/A genotypes (nonsmokers, p = 0.0022, and smokers, p = 0.0402). The reporter gene assay showed significantly lower reporter activities in the presence of interferon-gamma for the 38A construct than the 38G construct (p = 0.0177). The G38A polymorphism in the CC10 gene may influence protein expression and be associated with the development of progressive sarcoidosis.

DOI

Molecules regulating the function of thymic epithelial cells

Clinical Immunology 2004年

Inhibition of MAP kinase activity moderates changes in expression and function of Cx32 but not claudin-1 during DNA synthesis in primary cultures of rat hepatocytes

Takashi Kojima, Toshinobu Yamamoto, Mengdong Lan, Masaki Murata, Ken-Ichi Takano, Mitsuru Go, Shingo Ichimiya, Hideki Chiba, Norimasa Sawada

Medical Electron Microscopy ( Springer Japan ) 37 ( 2 ) 101 - 113 2004年

The signal transduction pathways and activation of the MAP kinase or PI3 kinase signaling cascade regulate a variety of cellular processes, including proliferation and differentiation in hepatocytes. To elucidate the mechanisms of signal transmission required for the regulation of gap and tight junctions during DNA synthesis in rat hepatocytes, we determined changes of expression and function of gap and tight junctions of cells grown in primary culture, using inhibitors of signaling pathways for MAP kinase (PD98059) and PI3 kinase (LY294002). During the stimulation of DNA synthesis induced by epidermal growth factor (EGF), immunoreactivity and mRNAs of gap junction protein Cx32 and of tight junction protein claudin-1 markedly decreased with reduction of gap junctional intercellular communication (GJIC) and the fence function of tight junctions. In Western blots, whole-cell lysate of claudin-1 protein decreased and phosphorylated Cx32 protein in the insoluble fraction of Triton X-100 increased during the stimulation of DNA synthesis. During reinhibition of DNA synthesis, the changes of Cx32 and claudin-1 returned to control levels, as did both functions. In treatment with the inhibitors before DNA synthesis, PD98059 inhibited the changes of expression and function of Cx32, but not claudin-1, without inhibition of cell growth, whereas LY294002 completely inhibited cell growth. These findings indicate that the PI3 kinase pathway rather than the MAP kinase pathway plays an important role for EGF-induced proliferation of rat hepatocytes, and that changes of Cx32 in hepatocytes during the stimulation of DNA synthesis may be in part controlled through MAP kinase. Furthermore, Cx32, but not claudin-1, protein may be a target of activated MAP kinase in hepatocytes.

DOI PubMed

胸腺上皮細胞機能を制御する分子群

臨床免疫 2004年

Chymase-positive mast cells in small sized adenocarcinoma of the lung

M Nagata, N Shijubo, AF Walls, S Ichimiya, S Abe, N Sato

VIRCHOWS ARCHIV ( SPRINGER-VERLAG ) 443 ( 4 ) 565 - 573 2003年10月

Mast cells accumulate in angiogenesis-dependent situations of lung adenocarcinoma. Human mast cells are divided into two major subsets: MCT (mast cells with immunoreactivity for tryptase but not chymase) and MCTC (reactive for tryptase and chymase). Chymase is an important mediator of tissue remodeling, but research into chymase-containing mast cell subpopulations has been hampered by the lack of reagents suitable for use with formalin-fixed tissue. We stained chymase using CC1 antibody in 66 cases of small sized lung adenocarcinoma as well as CD34 and tryptase. There were significant positive correlations of microvessel counts with MCT-type and MCTC-type mast cell counts in lung adenocarcinomas. When analyzed according to Noguchi's classification, MCT-type and MCTC-type mast cells were significantly increased in Noguchi type-C tumors [localized bronchioloalveolar carcinoma (LBAC) with active fibroblastic proliferation] compared with in Noguchi type-A (LBAC) plus type-B tumors (LBAC with alveolar collapse). Members in the high-count group of MCTC-type but not MCT-type mast cells showed a significantly worse outcome than those in the low-count group in LBACs. Counting chymase-positive (MCTC-type) mast cells in tumor stroma may be a good prognosis predictor for LBACs, especially Noguchi type-C tumors.

DOI

Histone H2AX sensitizes glioma cells to genotoxic stimuli by recruiting DNA double-strand break repair proteins

H Momota, S Ichimiya, N Kondo, T Kikuchi, T Torigoe, T Yamaki, K Houkin, N Sato

INTERNATIONAL JOURNAL OF ONCOLOGY ( PROFESSOR D A SPANDIDOS ) 23 ( 2 ) 311 - 315 2003年08月

Glioblastoma is a life-threatening tumor in the human brain despite the fact that radio-chemotherapy inducing DNA damage has been improved in the last decade. Various studies focusing on the enhancement of the susceptibility of glioblastoma cells to DNA damage have been reported, which are aimed at more efficient treatment for the tumor. In this study, we show that radioresistant T98G glioblastoma cells can develop sensitivity to DNA damage induced by irradiation and etoposide as a result of the introduction of a DNA repair-associated historic, H2AX. Interestingly, when H2AX-transformed T98G cells were irradiated, Brca1 and Nbs1 were readily recruited in DNA double-strand break (DSB) foci and showed the G2/M-phase arrest of the cell cycle. Moreover, up-regulation of Brcal was observed in H2AX-T98G cells after exposure to irradiation. Together with the evidence that H2AX transfection does not affect growth activities of non-tumor cells under genotoxic stimuli, this suggests that H2AX gene transfer would provide a new modality for radio-chemotherapy for glioblastomas, probably through overcoming the instability of the genome, and that Brca1 and Nbs1 might be crucial in this methodology.

Role of the p38 MAP-kinase signaling pathway for Cx32 and claudin-1 in the rat liver

T Kojima, T Yamamoto, M Murata, M Lan, KI Takano, M Go, S Ichimiya, H Chiba, N Sawada

CELL COMMUNICATION AND ADHESION ( TAYLOR & FRANCIS LTD ) 10 ( 4-6 ) 437 - 443 2003年07月

Liver regeneration and cholestasis are associated with adaptive changes in expression of gap and tight junctions through signal transduction. The roles of stress responsitive MAP-kinase, p38 MAP-kinase, in the signaling pathway for gap junction protein, Cx32, and tight junction protein, claudin-1, were examined in rat liver in vivo and in vitro , including regeneration following partial hepatectomy and cholestasis after common bile duct ligation. Changes in the expression and function of Cx32 and claudin-1 in hepatocytes in vivo were studied using the p38 MAP-kinase inhibitor SB203580. Following partial hepatectomy and common bile duct ligation, down-regulation of Cx32 protein was inhibited by SB203580 treatment. Up-regulation of claudin-1 protein was enhanced by SB203580 treatment after partial hepatectomy but not common bile duct ligation. However, no change of the Ki-67 labeling index (which is a marker for cell proliferation) in the livers treated with SB203580, was observed compared to that without SB203580 treatment. In primary cultures of rat hepatocytes, however, treatment with a p38 MAP-kinase activator, anisomycin, decreased Cx32 and claudin-1 protein levels. p38 MAP-kinase may be an important signaling pathway for regulation of gap and tight junctions in hepatocytes. Changes of gap and tight junctions during liver regeneration and cholestasis are shown to be in part controlled via the p38 MAP-kinase signaling pathway and are independent of cell growth.

DOI

Frequent beta-catenin alteration in gallbladder carcinomas

Y Kimura, T Furuhata, M Mukaiya, C Kihara, M Kawakami, K Okita, Y Yanai, H Zenbutsu, M Satoh, S Ichimiya, K Hirata

JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH ( APSIT ASSOC PROM STUD IMMUNOL TUMOR ) 22 ( 2 ) 321 - 328 2003年06月

To investigate the contribution of beta-catenin to the development of gallbladder carcinoma, genetic alteration in beta-catenin gene, ctnnb-1 and subcellular localization of beta-catenin protein were searched. Mutational analysis of exon 3 in ctnnb-1, which encodes the serine/threonine residues for GSK3beta phosphorylation sites, was performed for 21 gallbladder carcinomas affected with/without the pancreaticobiliary malunion, PBM, and 6 non-cancerous tissues affected with PBM. We also analyzed subcellular localization of beta-catenin protein in all cases immunohistochemically. Nucleotide sequencing analysis revealed that none of them carried mutations that altered amino acid residues in the potential GSK3beta phophorylation sites, but one nucleotide substitution was found. We also analyzed subcellular localization of beta-catenin protein in all cases immunohistochemically, and confirmed its accumulation in both the nucleus and cytoplasm in 10 out of 21 cancer tissues, while the non-cancerous tissues which were affected with PBM and histologically diagnosed as hyperplasia or dysplasia displayed intense membranous staining. A significant correlation between cytoplasmic or nuclear beta-catenin immunoreactivity and clinicopathological status of gallbladder carcinomas was found, especially in the poorer histological differentiation grade(p<0.05). In conclusion our results suggested that β-catenin alteration might be a minor contributor to the development of gallbladder carcinomas through abnormal Wnt-wingless signalling, however, decreased membranous expression of β-catenin might be correlated to carcinoma progression through loss of cell adhesive function in E-cadherin-catenin fashion.

Rapidly growing early gastric cancer with microsatellite instability

K Yamashita, N Kato, H Takahashi, H Shimizu, H Suzuki, S Motoya, Y Arimura, T Endo, H Ura, S Ichimiya, K Imai

JOURNAL OF GASTROENTEROLOGY ( SPRINGER-VERLAG TOKYO ) 38 ( 2 ) 170 - 174 2003年02月

A 77-year-old man underwent gastrointestinal endoscopy that revealed a small flat elevated lesion in the gastric antrum. Endoscopically, we assessed the tumor as intramucosal cancer or adenoma, and biopsy specimens were diagnosed as showing borderline malignancy. At the second examination, performed 6 months later, the elevated lesion had grown, showing remarkable changes in its appearance, and a diagnosis of adenocarcinoma was confirmed pathologically. The patient underwent distal gastrectomy about 8 months after the first examination, and the tumor in the resected specimens showed a moderately differentiated adenocarcinoma invading through the entire submucosal layer, with metastasis to a regional lymph node. Microsatellite analysis of this early gastric cancer disclosed mutations in all six markers examined, indicating high-level microsatellite instability (NISI-H). The tumor also showed frameshift mutations of TGFbetaRII and BAX genes, as well as hypermethylation of the hMLH1 promoter. These results suggest that a deficiency of the mismatch repair system played a critical role in the progression of this cancer.

DOI PubMed

T-cell receptor variable gamma chain gene expression in the interaction between rat gamma delta-type T cells and heat-shock protein 70-like molecule

T Ichinohe, S Ichimiya, A Kishi, Y Tamura, N Kondo, G Ueda, T Torigoe, A Yamaguchi, H Hiratsuka, Hirai, I, G Kohama, N Sato

MICROBIOLOGY AND IMMUNOLOGY ( CENTER ACADEMIC PUBL JAPAN ) 47 ( 5 ) 351 - 357 2003年

We previously reported that rat T-cell receptor (TCR) Vdelta6 of T-cell hybridomas was preferentially involved in recognition of the cell surface-expressed 70 kDa rat heat-shock cognate (hsc70, a constitutively expressed member of the hsp 70 family) protein-like molecule (#067 molecule). In the present study, we analyzed usage of the TCR Vgamma family of #067-restricted T-cell hybridomas. Our data indicated that most of these hybridomas expressed transcripts of TCR Vgamma1 and/or Vgamma2. However, some of the Vgamma2 transcripts were out-of-frame, suggesting that the TCR Vgamma1 family may be important for the recognition of #067-defined molecules. TCR Vgamma1 transcripts were detected in not only #067-restricted T-cell hybridomas, but #067-non restricted ones as well. However, V-J nucleotide sequences of #067-restricted and #067-non restricted T-cell hybridomas suggested that #067-restricted T-cell hybridomas showed limited insertion of nucleotide stretch as compared with #067-non restricted ones. In terms of amino acids, only one amino acid was added in #067-restricted T-cell hybridomas, whereas two or three amino acids were added in #067-non restricted ones. These data suggest that the heterodimer of the TCR relatively short stretch form of Vgamma1 molecule and TCR Vdelta6 may participate in recognition of the #067 molecule.

Immunohistochemical analysis of the p53 family members in human craniopharyngiomas

Hiroyuki Momota, Shingo Ichimiya, Tatsuru Ikeda, Toshiaki Yamaki, Tomoki Kikuchi, Kiyohiro Houkin, Noriyuki Sato

Brain Tumor Pathology 20 ( 2 ) 73 - 77 2003年

Craniopharyngiomas are intracranial tumors that usually arise in the site around the sella turcica. They are composed of distinctive sheets of epithelial cells showing adamantinomatous or squamous-papillary histologic types. Because little is known about the tumorigenesis of craniopharyngiomas, we retrieved samples from 15 tumor cases to investigate the functional significance of the p53 family of transcription factors, which are known to be expressed in various human epithelia. Immunohistochemical analysis of these cases demonstrated similar expression profiles of p53 family members in the two histologic types of the tumor i.e., strong nuclear expression of p63 was observed in all cell layers, and moderate to intense nuclear expression of p73 was observed in the basal cell layers. In contrast to p63 and p73, the reactivity of an archetypal tumor suppressor, p53, was occasional and weak in the two histologic types. Because p63 was widely expressed in the tumors, reverse transcription-polymerase chain reaction (RT-PCR) analysis was conducted to elucidate which spliced variant of p63 was expressed. The results showed that ANp63, lacking a terminal transactivation domain of p63, was the dominant isoform. Together with the reported evidence that the ANp63 isoform is highly expressed in human squamous-cell carcinomas, these data suggest that the cellular architecture characteristic of the expression of p53 family members may be required for the histogenesis of craniopharyngiomas, where ANp63 has a possible role in maintaining proliferative activity of the tumor cells, like squamous-cell carcinomas in other tissues.

DOI PubMed CiNii

Improved generation of HLA class I/peptide tetramers

Y Sato, H Sahara, T Tsukahara, M Kondo, Y Hirohashi, Y Nabeta, S Kawaguchi, H Ikeda, T Torigoe, S Ichimiya, Y Tamura, T Wada, T Yamashita, M Goto, H Takasu, N Sato

JOURNAL OF IMMUNOLOGICAL METHODS ( ELSEVIER SCIENCE BV ) 271 ( 1-2 ) 177 - 184 2002年12月

As a tetrameric major histocompatibility complex (MHC) class I-peptide complex (tetramer) is capable of detecting antigen-specific cytotoxic T lymphocyte (CTL) by flow cytometry, significant information about the generation of in vivo immunity can be obtained. It is, however, difficult to make a soluble wild type of MHC class I heavy chain by the prokaryotic expression system. Therefore, we developed a new method for making soluble mutant HLA-A*2402 heavy chain. In this method, signal sequences were deleted, and the codon was changed to silent mutated nucleotide sequences that bacteria could use as preferable codon. When purified mutant HLA-A*2402 molecules were examined for the protein generation by SDS-polyacrylamide gel electrophoresis (PAGE) and western blotting using anti-HLA class I monoclonal antibody (mAb) as compared with wild type, a large amount of mutant heavy chain could be detected. In contrast, the expression of wild-type stable HLA-A*2402 heavy chain molecule was not detected in this system. Consequently, by using mutant HLA-A*2402/peptide tetramers, CTL precursors (CTLp) that specifically recognize antigenic peptide derived from the X;18 chromosomal translocations of synovial sarcoma were detected in patients' PBL. (C) 2002 Elsevier Science B.V. All rights reserved.

DOI PubMed CiNii

Detection and induction of CTLs specific for SYT-SSX-derived peptides in HLA-A24(+) patients with synovial sarcoma

Y Sato, Y Nabeta, T Tsukahara, Y Hirohashi, R Syunsui, A Maeda, H Sahara, H Ikeda, T Torigoe, S Ichimiya, T Wada, T Yamashita, H Hiraga, A Kawai, T Ishii, N Araki, A Myoui, S Matsumoto, T Umeda, S Ishii, S Kawaguchi, N Sato

JOURNAL OF IMMUNOLOGY ( AMER ASSOC IMMUNOLOGISTS ) 169 ( 3 ) 1611 - 1618 2002年08月

To investigate the immunogenic property of peptides derived from the synovial sarcoma-specific SYT-SSX fusion gene, we synthesized four peptides according to the binding motif for HLA-A24. The peptides, SS391 (PYGYDQIMPK) and SS393 (GYD QIMPKK), were derived from the breakpoint of SYT-SSX, and SS449a (AWTHRLRER) and SS449b (AWTHRLRERK) were from the SSX region. These peptides were tested for their reactivity with CTL precursors (CTLps) in 16 synovial sarcoma patients using HLA-A24/SYT-SSX peptide tetramers and also for induction of specific CTLs from four HLA-A24(+) synovial sarcoma patients. Tetramer analysis indicated that the increased CTLp frequency to the SYT-SSX was associated with pulmonary metastasis in synovial sarcoma patients (p < 0.03). CTLs were induced from PBLs of two synovial sarcoma patients using the peptide mixture of SS391 and SS393, which lysed HLA-A24(+) synovial sarcoma cells expressing SYT-SSX as well as the peptide-pulsed target cells in an HLA class I-restricted manner. These findings suggest that aberrantly expressed SYT-SSX gene products have primed SYT-SSX-specific CTLps in vivo and increased their frequency in synovial sarcoma patients. The identification of SYT-SSX peptides may offer an opportunity to design peptide-based immunotherapeutic approaches for HLA-A24(+) patients with synovial sarcoma.

DOI

A gene encoding human gastric signet ring cell carcinoma antigen recognized by HLA-A31-restricted cytotoxic T lymphocytes

H Sahara, Y Nabeta, T Torigoe, Y Hirohashi, S Ichimiya, Y Wada, N Takahashi, K Jimbow, T Yajima, N Watanabe, K Kikuchi, N Sato

JOURNAL OF IMMUNOTHERAPY ( LIPPINCOTT WILLIAMS & WILKINS ) 25 ( 3 ) 235 - 242 2002年05月

We previously reported acid-extracted natural antigenic peptide (F4.2[YSWMDISCWI]) of a gastric signet ring cell carcinoma HST-2 cells, recognized by HLA-A*31012-restricted autologous cytotoxic T lymphocytes, TcHST-2 line. In this study, the full-length cDNA (1101 bp), termed c98, predicting a protein composed of 170 amino acids was obtained. Because TcHST-2 cells could lyse the HLA-A31 antigen (+) allogeneic tumor cells that were introduced with c98 gene, this gene was suggested to possess antigenicity. Beginning at N-terminal 61 amino acid, the N-terminal six amino acid sequence that is completely identical to F4.2 was present in c98; however, a sequence of four amino acids in C-terminal was not found. Nevertheless, this peptide, c98(61-70), seemed to be immunogenic, because cells pulsed with c98(61-70) peptide were lysed in a dose-dependent manner by TcHST-2 cells. The c98 gene was expressed ubiquitously in tumor cells as well as in normal tissues. However, some tumor cells, including HST-2 cells, expressed this antigen in a high content, and such cells were lysed by TcHST-2 cells in the context of HLA-A31 antigen. However, TcHST-2 cells did not lyse cells that expressed lower amounts of c98 than HST-2 cells. These data suggested that c98-gene product and/or C98(61-70) peptides could be used as a candidate for tumor vaccines in cancer immunotherapy.

DOI

p73 is expressed in human thymic epithelial cells

S Ichimiya, T Kojima, H Momota, N Kondo, T Ozaki, A Nakagawara, ML Toribio, M Imamura, N Sato

JOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY ( HISTOCHEMICAL SOC INC ) 50 ( 4 ) 455 - 462 2002年04月

The thymus is a heterogeneous immune organ in which immature T-cells develop and eventually specialize to make certain immune responses of their own. Among various types of stromal cells in the thymus, thymic epithelial cells (TECs) have a crucially important function for presenting self-antigens and secreting cytokines to thymocytes for their maturation into T-cells. In this study we show that the p73 gene, a homologue of the tumor suppressor gene p53, was expressed in the nucleus of the human TEC in vivo and in TEC lines in vitro. Because p73 has the capacity to be a transactivator like p53, it may contribute to T-cell development in the context of TEC biology as regulated in the cell cycle and apoptosis.

迅速診断の標本作製に最良な固定法の選定

浅沼広子, 東恭悟, 一宮慎吾, 佐藤昌明

臨床検査 ( 株式会社医学書院 ) 46 ( 1 ) 77 - 81 2002年

DOI

微細組織の遺伝子研究

一宮慎吾, 佐藤昇志

北海道醫學雜誌 = Acta medica Hokkaidonensia ( 北海道大学 ) 77 ( 2 ) 139 - 41 2002年

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