KINDAI UNIVERSITY


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MASAKI Hideyuki

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FacultyDepartment of Biomedical Engineering / Graduate School of Biology-Oriented Science and Technology
PositionAssociate Professor
Degree
Commentator Guidehttps://www.kindai.ac.jp/meikan/1355-masaki-hideyuki.html
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Last Updated :2020/09/10

Education and Career

Education

  •  - 1992 , Kindai University
  •  - 1985 , Kindai University, Faculty of Medicine
  •  - 1992 , Kinki University, Graduate School, Division of Medicine
  •  - 1985 , Kinki University, Faculty of Medicine

Academic & Professional Experience

  •   2015 04 ,  - 現在, Associate Professor, Department of Biomedical Engineering, Kinki University Faculty of Biology-Oriented Science and Technology
  •   2002 ,  - 2015 03 , Faculty of Medicine, Kindai University
  •   2002 ,  - 2015 03 , Lecturer, Department of Biochemistry, Kinki University Faculty of Medicine
  •   2001 ,  - 2002 , Faculty of Medicine, Kindai University
  •   2001 ,  - 2002 , Research Associate, Department of Biochemistry, Kinki University Faculty of Medicine
  •   1998 ,  - 2001 , Postdoctoral research fellow, Diabetes Division, University of Massachusetts
  •   1992 ,  - 1998 , Faculty of Medicine, Kindai University
  •   1992 ,  - 1998 , Research Associate, Department of Microbiology, Kinki University Faculty of Medicine

Research Activities

Research Areas

  • Life sciences, Immunology
  • Life sciences, Virology

Research Interests

  • Immunology, Virology

Published Papers

  • Human monoclonal antibodies against West Nile virus from Japanese encephalitis-vaccinated volunteers., Tatsuhiko Ozawa, Hideyuki Masaki, Tomohiko Takasaki, Ikuko Aoyama, Takahiro Yumisashi, Atsushi Yamanaka, Eiji Konishi, Yoh Ohnuki, Atsushi Muraguchi, Hiroyuki Kishi, Antiviral research, Antiviral research, 154, 58 - 65, Jun. 2018 , Refereed
    Summary:West Nile virus (WNV) is a positive-sense single-stranded RNA flavivirus belonging to the Japanese encephalitis virus (JEV) serocomplex of the Flaviviridae family and causes mosquito-borne infections. Although most human infection cases are asymptomatic, approximately one in 150 infected individuals develops meningoencephalitis, with a mortality rate of 4-14%. While the development of human neutralizing antibody therapeutics against WNV is strongly anticipated, WNV is difficult to study in conventional laboratories due to its high safety level requirement. In this study, we established fully human WNV-neutralizing monoclonal antibodies from the peripheral blood mononuclear cells of inactivated-JEV-vaccinated individuals, and these antibodies exhibited WNV neutralization both in vitro and in vivo. Our results demonstrate a new antibody cross-reactivity strategy to develop immunological therapeutic reagents for WNV and other JEV serotype viruses.
  • Establishment and characterization of mouse T-cell clones reactive to rat xeno-antigens activated via the direct or indirect recognition pathway, Acta Medica Kinki University, Acta Medica Kinki University, 38(2), 101 - 109, Dec. 2013
  • Enhancement of MHC class I binding and immunogenic properties of the CTL epitope peptides derived from dengue virus NS3 protein by anchor residue replacement, Dengue Bulletin, Dengue Bulletin, 32, 99 - 109, Dec. 2008
  • Modification of the Anchor Residue to MHC Class I Augments CTL-Inducing Ability of Epitope Peptides Derived from Dengue Virus NS3 Protein, Dengue Bulletin, Dengue Bulletin, 30, 171 - 176, Dec. 2006
  • Induction of cytotoxic T lymphocytes by immunization with dengue virus derived, modified epitope peptide, using dendritic cells as a peptide delivery system, Dengue bulletin, Dengue bulletin, 28, 145 - 150, Dec. 2004
  • Definition of an epitope on Japanese encephalitis virus (JEV) envelope protein recognized by JEV-specific murine CD8(+) cytotoxic T lymphocytes, K Takada, H Masaki, E Konishi, M Takahashi, Kurane, I, ARCHIVES OF VIROLOGY, ARCHIVES OF VIROLOGY, 145(3), 523 - 534, 2000
    Summary:We defined an epitope on the Japanese encephalitis virus (JEV) envelope (E) protein recognized by CD8(+) cytotoxic T lymphocytes (CTLs). CTLs induced in JEV-infected BALB/c (H-2(d)) mice recognized E and/or premembrane (PrM) proteins, while CTLs in C57BL/6J (H-2(b)) and C3H/HeJ (H-2(k)) mice did not. JEV-specific CTLs had a phenotype of CD3(+) CD4(-) CD8(+). Twenty-four 9-amino acid (a.a.) peptides, which had binding motifs for H-2K(d), H-2L(d) or H-2D(d), were synthesized according to the amino acid sequences of PrM and E proteins. CTLs induced by JEV infection recognized only the peptide K-3. Immunization of BALB/c mice with only a group of peptides including K-3 induced CTLs which recognized the homologous K-3 peptide, while immunization with other peptides did not. The peptide K-3 had a binding motif for H-2K(d). This is consistent with the finding that JEV-specific CTLs in BALB/c mice was H-2K(d)-restricted. These results indicate that the epitope recognized by CTLs in BALB/c mice is located between a.a. 60 and 68 on the E protein, corresponding to an a.a. sequence of CYHASVTDI.
  • Establishment and characterization of an anti-idiotypic CD4(+) CD8(-) T cell line to murine anti-alpha(1->3) dextran antibody, H Masaki, K Irimajiri, A Horiuchi, J Yamaguchi, T Toyosaki, R Suzuki, Kurane, I, CELLULAR IMMUNOLOGY, CELLULAR IMMUNOLOGY, 174(2), 180 - 189, Dec. 1996
    Summary:It is known that anti-alpha(1 --> 3) dextran antibodies of BALB/c mice are ordinarily of distinctive idiotypes (Id), one of which is the individual idiotype (IdI) that is represented by J558 or M104E to myeloma protein. In the present study, we established T cell line of Th1 type which recognized the Id of anti-alpha(1 --> 3) dextran antibody, and investigated its specificity and functions. The T cell line, named J-2R, had a phenotype of CD3(+) CD4(+) CD8(-) and expressed alpha beta-T cell receptors (TcR). J-2R proliferated in response to J558 in an I-E(d)-restricted manner but did not respond to M104E which had substitution at amino acids 100 and 101. We confirmed that J-2R recognized J558 IdI, using synthetic peptides corresponding to two serial amino acid residues, Arg(100) and Tyr(101), spanning the J558 IdI in the third hypervariable region (hv3) of the heavy chain. alpha(1 --> 3) dextran-binding B cells which were isolated from dextran-immunized mice activated J-2R, but B cells from nonimmune mice did not. J-2R produced IL-2, IFN-gamma and IL-6, but did not produce IL-4, IL-5, or IL-10. Furthermore, J-2R inhibited the growth of J558 myeloma cells inoculated to the syngeneic mice in vivo. These findings suggest that Id-specific CD4(+) T cells, J-2R, are involved in Id network and may play a role in vivo. J-2R is useful for analysis of the role of the Id-specific helper T cells in immune network because J558 IdI is frequently present on anti-alpha(1 --> 3) dextran antibodies. (C) 1996 Academic Press, Inc.
  • CD3 down-regulating factor in patients with adult T cell leukemia, Yasuhiro Maeda, Mitsuhiro Matsuda, Satosi Morita, Hideyuki Masaki, Chikashi Shirakawa, Fusanari Horiuchi, Atsuko Koyama, Hiroyuki Hamazaki, Takuya Fujimoto, Kiyohiro Irimajiri, Atsushi Horiuchi, Japanese Journal of Clinical Immunology, Japanese Journal of Clinical Immunology, 16(2), 118 - 125, Jan. 01 1993
    Summary:It is known that human lymphotropic virus type I (HTLV-I) is closely associated with adult T cell leukemia (ATL). The immunological abnormality of T lymphocytes in patients with ATL is characterized by their abnormal expression of the 55 kDa chain of the receptor for interleukin 2 (IL-2 R/p55 (Tac)), and the down-regulation of CD 3 antigen. HTLV-I gene products such as p 40 tax or ATL-derived factor (ADF) have been shown to enhance the expression of IL-2 R/p55 (Tac). However, the mechanism of down-regulation of CD 3 antigen on T lymphocytes in ATL patients still remains unclear. We found that CD 3 expression on peripheral blood mononuclear cells (PBMC) in healthy individuals was decreased significantly by treatment with sera and cell culture supernatants from ATL patients whose CD 3 expression on PBMC was decreased markedly, but not by sera and cell culture supernatants from ATL patients whose CD 3 expression was normal. Gel-chromatography for cell culture supernatant showed that CD 3 down-regulating activity was fractioned in the fraction number 11 which arrowed 40~60 kDa. Next, after culture with various cytokines (IL-1, IL-2, IL-4, IL-6, IFN γ and TNF α), the expression of CD 3 on normal PBMC was not reduced significantly. Furthermore, by treatment of cell culture supernatant with various anti-cytokine antibody, the expression of CD 3 antigen on normal PBMC was down-regulated. As mentioned above, there are novel factor (s) with CD 3 down-regulating activity in the sera and cell culture supernatants of those acute ATL patients. In this study, we tried to clarify the mechanism of down-regulation of CD 3 expression on ATL cells, based on the finding of soluble factor (s) down-regulating CD 3 molecule. © 1993, The Japan Society for Clinical Immunology. All rights reserved.
  • Induction of specific and flavivirus-Cross-reactive CTLs by immunization with a single dengue virus-derived CTL epitope peptide, Hideyuki Masaki, Yoshiki Fujii, Chiaki Wakasa-Morimoto, Tomoko Toyosaki-Maeda, Kiyohiro Irimajiri, Takanori T. Tomura, Ichiro Kurane, VIRUS RESEARCH, VIRUS RESEARCH, 144(1-2), 188 - 194, Sep. 2009
    Summary:Specificities of cytotoxic T lymphocyte (CTL) effector cells induced in BALB/c mouse by immunization with the single modified CTL epitope peptide derived from NS3 of dengue virus types 1 and 3, or that of dengue virus types 2 and 4 were examined. The effector cells included CTLs specific for the epitope peptide used for immunization and those cross-reactive to epitope peptides of other flaviviruses. A CTL clone, 2F7, was established from the effector cells. The clone 2F7 was specific for the epitope peptide used for immunization. Recognition by the effector cells was remarkably impaired by amino acid substitutions at positions 3, 5, and 6 of the epitope peptides. These results indicate that immunization with a single CTL epitope peptide of dengue viruses induces serotype-specific CTLs as well as CTLs cross-reactive to the other flaviviruses, and that the a.a. residues at positions 3, 5, and 6 are critical for cross-reaction. (C) 2009 Elsevier B.V. All rights reserved.
  • Arthritis and pneumonitis produced by the same T cell clones from mice with spontaneous autoimmune arthritis, Chiaki Wakasa-Morimoto, Tomoko Toyosaki-Maeda, Takaji Matsutani, Ryu Yoshida, Shino Nakamura-Kikuoka, Miki Maeda-Tanimura, Hiroyuki Yoshitomi, Keiji Hirota, Motomu Hashimoto, Hideyuki Masaki, Yoshiki Fujii, Tsuneaki Sakata, Yuji Tsuruta, Ryuji Suzuki, Noriko Sakaguchi, Shimon Sakaguchi, INTERNATIONAL IMMUNOLOGY, INTERNATIONAL IMMUNOLOGY, 20(10), 1331 - 1342, Oct. 2008
    Summary:SKG mice, a newly established model of rheumatoid arthritis (RA), spontaneously develop autoimmune arthritis accompanying extra-articular manifestations, such as interstitial pneumonitis. To examine possible roles of T cells for mediating this systemic autoimmunity, we generated T cell clones from arthritic joints of SKG mice. Two distinct CD8(+) clones were established and both showed in vitro autoreactivity by killing syngeneic synovial cells and a variety of MHC-matched cell lines. Transfer of each clone to histocompatible athymic nude mice elicited joint swelling and histologically evident synovitis accompanying the destruction of adjacent cartilage and bone. Notably, the transfer also produced diffuse severe interstitial pneumonitis. Clone-specific TCR gene messages in the inflamed joints and lungs of the recipients gradually diminished, becoming hardly detectable in 6-11 months; yet, arthritis and pneumonitis continued to progress. Thus, the same CD8(+) T cell clones from arthritic lesions of SKG mice can elicit both synovitis and pneumonitis, which chronically progress and apparently become less T cell dependent in a later phase. The results provide clues to our understanding of how self-reactive T cells cause both articular and extra-articular lesions in RA as a systemic autoimmune disease.
  • Anti-mouse CD154 antibody treatment facilitates generation of mixed xenogeneic rat hematopoietic chimerism, prevents wasting disease and prolongs xenograft survival in mice, H Masaki, MC Appel, L Leahy, J Leif, L Paquin, LD Shultz, JP Mordes, DL Greiner, AA Rossini, XENOTRANSPLANTATION, XENOTRANSPLANTATION, 13(3), 224 - 232, May 2006
    Summary:Background: The induction of xenogeneic hematopoietic chimerism is an attractive approach for overcoming the host response to xenografts, but establishing xenogeneic chimerism requires severe myeloablative conditioning of the recipient. The goal of this study was to determine if co-stimulation blockade would facilitate chimerism and xenograft tolerance in irradiation-conditioned concordant recipients. Methods: Wistar Furth rat bone marrow (BM) cells were injected into irradiation-conditioned C57BL/6 mice with or without co-administration of anti-mouse CD154 monoclonal antibody (mAb). Chimerism was quantified by flow cytometry, and mice were transplanted with WF rat skin and islet xenografts. Results: Blockade of CD40-CD154 interaction facilitated establishment of xenogeneic chimerism in mice conditioned with 600 cGy irradiation. Anti-CD154 mAb was not required for establishment of chimerism in mice treated with 700 cGy. However, mice irradiated with 700 cGy but not treated with anti-CD154 mAb developed a "graft-versus-host disease (GVHD)-like" wasting syndrome and died, irrespective of their development of chimerism. Xenogeneic chimeras established with irradiation and anti-CD154 mAb treatment exhibited prolonged skin and, in many cases, permanent islet xenograft survival. Chimerism was unstable and eventually lost in most recipients. Skin xenografts were rejected even in mice that remained chimeric, whereas most islet xenografts survived to the end of the observation period. Conclusions: Blockade of host CD40-CD154 interaction facilitates the establishment of xenogeneic chimerism and prevents wasting disease and death. Chimerism permits prolonged xenograft survival, but chimerism generated in this way is unstable over time. Skin xenografts are eventually rejected, whereas most islet xenografts survive long term and perhaps permanently.
  • Induction of cytotoxic T lymphocytes of heterogeneous specificities by immunization with a single peptide derived from influenza A virus, H Masaki, M Tamura, Kurane, I, VIRAL IMMUNOLOGY, VIRAL IMMUNOLOGY, 13(1), 73 - 81, 2000
    Summary:We examined whether immunization with a single peptide induces cytotoxic T lymphocytes (CTLs) of heterogeneous specificities in vivo, Immunization of BALB/c mice with the peptide H2:529-537, which corresponded to amino acid residues 529-537 on the HA2 subunit transmembrane region of influenza A/Jap virus (H2N2) and possessed an H-2K(d)-binding motif, induced CD8(+)CD4(-) CTLs. These CTLs lysed influenza A/Jap virus-infected target cells as well as those pulsed with the H2:529-537 peptide, H2:529-537 peptide-induced CTLs also lysed to lower but significant levels the target cells pulsed with the H1:533-541 peptide, which corresponded to amino acid residues 533-541 on the HA2 subunit transmembrane region of influenza A/PR/8 virus (H1N1) and were compatible to H2:529-537. Immunization with the H1:533-541 peptide, which also possessed an H-2K(d)-binding motif, induced CTLs in vivo, H1:533-541-induced CTLs lysed influenza A/PR/8 virus-infected target cells and those pulsed with the peptide H1:533-541. Subtype cross-reactive CTLs to the H2:529-537 peptide were not induced by immunization with the H1:533-541 peptide, Two peptides, H2:3S and H2:7S, which had one amino acid substitution, serine at the third and seventh positions, respectively, induced CTLs that lysed target cells pulsed with the respective peptides to the highest levels. These results indicate that immunization with a single peptide induces CTLs of heterogeneous specificities in vivo.
  • DETECTION OF MINIMAL RESIDUAL DISEASE USING CLONOSPECIFIC PRIMERS FOR CDRIII IN PATIENTS WITH ACUTE B-LYMPHOCYTIC-LEUKEMIA WITH OR WITHOUT PHILADELPHIA-CHROMOSOME - POSSIBILITY OF CLINICAL-APPLICATION AS A TOOL FOR IMPROVING PROGNOSIS, Y MAEDA, F HORIUCHI, S MORITA, M MATSUDA, C SHIRAKAWA, H MASAKI, A KOYAMA, H HAMAZAKI, T FUJIMOTO, K IRIMAJIRI, A HORIUCHI, EXPERIMENTAL HEMATOLOGY, EXPERIMENTAL HEMATOLOGY, 22(9), 881 - 887, Aug. 1994
    Summary:We attempted to identify the minimal residual leukemic clone as related to the clinical course in patients with acute B lymphocytic leukemia (B-ALL). DNA was extracted from stored bone marrow slides, and the third complementarity determining region (CDRIII) was amplified by polymerase chain reaction (PCR) using primers with consensus sequences for V-H and J(H). After amplification of the CDRIII band, the DNA fragment of CDRIII was inserted into the cloning vector PUC118. After cloning, the DNA sequences for CDRIII were determined. Clonospecific DNA sequences in CDRIII were selected, and clonospecific primers for each patient were synthesized. Using the clonospecific primers, we carried out second-round PCR to detect minimal residual disease (MRD) during several stages of the clinical course. Basically, the sensitivity of detection for MRD was between 10(-4) and 10(-5) cells. Even when leukemic cells were not detected in the morphologic study, with this detection system, the MRD was identified as an amplified CDRIII band stained with ethidium bromide on agarose gel. After bone marrow transplantation (BMT), MRD was detected for at least 4 months. In this article, we discuss the difference in sensitivity of detection for MRD between the BCR-ABL fusion gene and CDRIII in Philadelphia chromosome-positive (Ph(+)) B-ALL, as well as the possible clinical application of this method to predict relapse and prognosis.
  • CD3 DOWN-REGULATING FACTOR IN SERA AND CULTURE SUPERNATANTS OF LEUKEMIC-CELLS FROM PATIENTS WITH ADULT T-CELL LEUKEMIA, M MATSUDA, Y MAEDA, C SHIRAKAWA, H MASAKI, A KOYAMA, F HORIUCHI, H HAMAZAKI, T FUJIMOTO, K IRIMAJIRI, A HORIUCHI, BRITISH JOURNAL OF HAEMATOLOGY, BRITISH JOURNAL OF HAEMATOLOGY, 83(2), 212 - 217, Feb. 1993
    Summary:Immunological abnormality of T lymphocytes in patients with adult T cell leukaemia (ATL) is characterized by abnormal expression of the 55 kD chain of the receptor for interleukin 2 (IL-2R/p55) (Tac), and the down-regulation of CD3 expression. Using serum and culture supernatants of leukaemic cells from ATL patients (Group A) whose CD3 expression was down-regulated and those (Group B) whose CD3 was not low, the possible mechanism of CD3 down-regulation on ATL cells was discussed. When PBMC from normal individuals were cultured with sera from ATL patients for 24 h, CD3 expression revealed by mean fluorescent intensity (MFI) was down-regulated by sera from ATL patients in Group A (MFI: Pt 1=51.6+/-4.5, Pt 2=48.0+/-6.9, control=96.5+/-6.6), not by sera from patients in Group B (MFI: Pt 3=105.5+/-7.9, Pt 4=102.5+/-8.3, control=96.5+/-6.6).When normal PBMC were cultured with supernatants of leukaemic cells from ATL patients in Group A, this CD3 down-regulating activity was also detected (MFI: Pt 1=78.0+/-10.2, Pt 2=70.6+/-8.7, control=94.0+/-6.6). By using gel-chromatography, the fractionated supernatants from ATL patients in Group A decreased CD3 expression of normal PBMC significantly (MFI: Pt 1=22.9+/-5.8, Pt 2=28.8+/-7.4, control=92.1+/-9.6). This CD3 down-regulating activity in fractionated supernatant was not inhibited by any lymphokine antibodies, anti-IL-1alpha antibody (Ab), anti-IL-1B Ab, anti-IL-2 Ab, anti-IL-3 Ab, anti-IL-4 Ab, anti-IL-6 Ab, anti-TNF-alpha Ab and anti-IFN-gamma Ab. Any known cytokines (IL-1, IL-2, IL-3, IL-4, IL-6, TNF-alpha and IFN-gamma) could not modulate CD3 expression of normal PBMC. These findings suggested that there are novel factor(s) with CD3 down-regulating activity in the serum and culture supernatant of ATL patient and those factor(s) are involved in progression of ATL.
  • GENERATION OF HELPER T-CELLS THAT RECOGNIZE A CROSS-REACTIVE IDIOTYPE THROUGH A NETWORK MECHANISM, H MASAKI, K IRIMAJIRI, MICROBIOLOGY AND IMMUNOLOGY, MICROBIOLOGY AND IMMUNOLOGY, 36(3), 279 - 295, 1992
    Summary:T cells that recognize the cross-reactive idiotype expressed on the heavy (H) chain of M104E (IgM, lambda(1)) were induced in BALB/c mice by immunization with Dextran B-1355. T cells derived from mice immunized with 1 mg of Dextran B-1355 showed a marked proliferative response against M104E, whereas T cells from mice immunized with Ficoll or lesser amounts of Dextran B-1355 did not. BCL1Id, which had an immunoglobulin isotype identical to M104E, did not induce proliferation of the T cells. These T cells also proliferated against J558 (IgA, lambda(1)) which shared the cross-reactive idiotype of the anti-alpha (1 --> 3) glucosidic linkage antibody with M104E on the H chain. The T cells proliferated more efficiently against F(ab')2-104E. Fab-104E and H104E, the H chain of M104E, than against intact M104E. The T cell proliferative response against the idiotype on M104E or even H104E required macrophages as antigen-presenting cells (APC) and the response was inhibited when APC were treated with NH4Cl or chloroquine, inhibitors of antigen processing. Moreover, anti-CD4 antibody or anti-Ia antibody inhibited the proliferative response. These results indicated that anti-idiotypic T cells of the helper type, which recognized a cross-reactive idiotype associated with Ia molecules in processed form, could be induced physiologically through a network mechanism.
  • INDUCTION OF ANTIIDIOTYPIC T-CELLS THROUGH A NETWORK MECHANISM, H MASAKI, C SHIRAKAWA, M MATSUDA, S MORITA, A KOYAMA, F HORIUCHI, H HAMAZAKI, T FUJIMOTO, Y MAEDA, K IRIMAJIRI, A HORIUCHI, IMMUNOLOGY LETTERS, IMMUNOLOGY LETTERS, 30(1), 107 - 112, Sep. 1991
    Summary:BALB/c mouse T cells that recognized the idiotype expressed on M104E(mu, lambda-1) were induced by immunization with Dextran B-1355. T cells derived from mice immunized with 1 mg of Dextran B-1355 showed a marked proliferative response against M104E, whereas T cells from mice immunized with Ficoll or smaller amounts of Dextran B-1355 did not. BCL1Id, which had an identical isotype, did not induce proliferation of T cells. The T cell proliferative response against the idiotype on M104E required macrophages as antigen-presenting cells. The proliferative response was inhibited when antigen-presenting cells were treated with NH4Cl or chloroquine, which are antigen-processing inhibitors. These results indicate that anti-idiotypic T cells which recognized processed idiotopes could be induced physiologically through a network mechanism.

Conference Activities & Talks

  • Human anti-WNV monoclonal antibodies established from JEV-vaccinated volunteers, MASAKI Hideyuki, PharmaLabo EXPO Academic Forum,   2019 07 03 , Reed Exhibitions Japan Ltd.
    Summary:We have established 3 human monolonal antibodies, which neutralize West Nile virus (WNV) as well as protect from WNV infection, from the volunteers immunized with WNV-related Japanese Encephalitis virus vaccine by using ISAAC technology.
  • Establishment of West Nile virus -neutralizing human monoclonal antibodies derived from the individuals vaccinated with inactivated Japanese encephalitis virus by ISAAC technology, MASAKI Hideyuki, 16th International Congress of Immunology,   2016 08
  • Induction of synovitis and interstitial pneumonitis by T cell clones from SKG mice with spontaneous arthritis,   2006 04
  • Analysis of the amino acid residues critical for antigen recognition of dengue virus NS3 - specific CTL clone induced by immunization with a single epitope peptide, 53rd Annual meeting of the American society of tropical medicine and hygiene,   2004 11 , 53rd Annual meeting of the American society of tropical medicine and hygiene
  • Induction of flavivirus cross-reactive CTLs by immunization with single dengue virus - derived CTL epitope peptide, 12th International congress of immunology and 4th Annual conference of FOCIS,   2004 07 , 12th International congress of immunology and 4th Annual conference of FOCIS
  • Costimulatory blockade with anti-CD40L Ab facilitates xenogeneic bone marrow chimerism and host survival,   2001 12
  • Costimulatory blockade with anti-CD40L Ab facilitates xenogeneic bone marrow chimerism and host survival, 30th Annual autumn immunology conference,   2001 11 , 30th Annual autumn immunology conference
  • Induction of flavivirus cross-reactive CTLs by immunization with single dengue virus - derived CTL epitope peptide, 12th International Congress of Immunology and 4th Annual Conference of FOCIS,   2004
  • Analysis of the amino acid residues critical for antigen recognition of dengue virus NS3 - specific CTL clone induced by immunization with a single epitope peptide, 53rd Annual Meeting of the American Society of Tropical Medicine and Hygiene,   2004
  • Costimulatory blockade with anti-CD40L Ab facilitates xenogeneic bone marrow chimerism and host survival, 30th Annual Autumn Immunology Conference,   2001
  • Establishment and analysis of fine specificity of anti-idiotypic helper T cell line against murine anti-α(1→3)dextran antibody, 9th International Congress of Immunology,   1995
  • Prevention of exit site infection by a removable silver-impacted silicone plate, International Faculty for Artificial Organs Taipei Symposium,   1995
  • The effect of molecules on cytotoxic and adhesion activity of LAK cells, 14th International Congress of Allergology and Clinical Immunology,   1991
  • Investigation about down-regulation of CD3 antigen in patients with adult T cell leukemia, 19th International Congress of Experimental Hematology,   1990
  • Cloning of myeloid leukemia specific gene, 19th International Congress of Experimental Hematology,,   1990
  • Detection of residual tumor cells in peripheral blood and bone marrow in patients with non-Hodgkin's lymphoma by southern blot analysis, 19th International Congress of Experimental Hematology,   1990

Misc

  • Induction of cytotoxic T lymphocytes by immunization with the dengue virus - derived epitope peptides with augmentation of binging affinity to MHC class I molecules, 22, 33, 40,   2006 12 , http://www.med.kindai.ac.jp/life/
  • Induction of flavivirus - cross-reactive CTLs by immunization with a single CTL epitope peptide derived from dengue viruses, 22, 41, 49,   2006 12 , http://www.med.kindai.ac.jp/life/
  • Induction of specific and flavivirus-Cross-reactive CTLs by immunization with a single dengue virus-derived CTL epitope peptide, Hideyuki Masaki, Yoshiki Fujii, Chiaki Wakasa-Morimoto, Tomoko Toyosaki-Maeda, Kiyohiro Irimajiri, Takanori T. Tomura, Ichiro Kurane, VIRUS RESEARCH, 144, 1-2, 188, 194,   2009 09 , 10.1016/j.virusres.2009.04.024
    Summary:Specificities of cytotoxic T lymphocyte (CTL) effector cells induced in BALB/c mouse by immunization with the single modified CTL epitope peptide derived from NS3 of dengue virus types 1 and 3, or that of dengue virus types 2 and 4 were examined. The effector cells included CTLs specific for the epitope peptide used for immunization and those cross-reactive to epitope peptides of other flaviviruses. A CTL clone, 2F7, was established from the effector cells. The clone 2F7 was specific for the epitope peptide used for immunization. Recognition by the effector cells was remarkably impaired by amino acid substitutions at positions 3, 5, and 6 of the epitope peptides. These results indicate that immunization with a single CTL epitope peptide of dengue viruses induces serotype-specific CTLs as well as CTLs cross-reactive to the other flaviviruses, and that the a.a. residues at positions 3, 5, and 6 are critical for cross-reaction. (C) 2009 Elsevier B.V. All rights reserved.
  • Arthritis and pneumonitis produced by the same T cell clones from mice with spontaneous autoimmune arthritis, Chiaki Wakasa-Morimoto, Tomoko Toyosaki-Maeda, Takaji Matsutani, Ryu Yoshida, Shino Nakamura-Kikuoka, Miki Maeda-Tanimura, Hiroyuki Yoshitomi, Keiji Hirota, Motomu Hashimoto, Hideyuki Masaki, Yoshiki Fujii, Tsuneaki Sakata, Yuji Tsuruta, Ryuji Suzuki, Noriko Sakaguchi, Shimon Sakaguchi, INTERNATIONAL IMMUNOLOGY, 20, 10, 1331, 1342,   2008 10 , 10.1093/intimm/dxn091
    Summary:SKG mice, a newly established model of rheumatoid arthritis (RA), spontaneously develop autoimmune arthritis accompanying extra-articular manifestations, such as interstitial pneumonitis. To examine possible roles of T cells for mediating this systemic autoimmunity, we generated T cell clones from arthritic joints of SKG mice. Two distinct CD8(+) clones were established and both showed in vitro autoreactivity by killing syngeneic synovial cells and a variety of MHC-matched cell lines. Transfer of each clone to histocompatible athymic nude mice elicited joint swelling and histologically evident synovitis accompanying the destruction of adjacent cartilage and bone. Notably, the transfer also produced diffuse severe interstitial pneumonitis. Clone-specific TCR gene messages in the inflamed joints and lungs of the recipients gradually diminished, becoming hardly detectable in 6-11 months; yet, arthritis and pneumonitis continued to progress. Thus, the same CD8(+) T cell clones from arthritic lesions of SKG mice can elicit both synovitis and pneumonitis, which chronically progress and apparently become less T cell dependent in a later phase. The results provide clues to our understanding of how self-reactive T cells cause both articular and extra-articular lesions in RA as a systemic autoimmune disease.
  • Enhancement of MHC class I binding and immunogenic properties of the CTL epitope peptides derived from dengue virus NS3 protein by anchor residue replacement, Masaki,H, Fujii,Y, Irimajiri,K, Tomura,T, Kurane,I, Dengue Bulletin, 32, 99,   2008
  • Anti-mouse CD154 antibody treatment facilitates generation of mixed xenogeneic rat hematopoietic chimerism, prevents wasting disease and prolongs xenograft survival in mice, H Masaki, MC Appel, L Leahy, J Leif, L Paquin, LD Shultz, JP Mordes, DL Greiner, AA Rossini, XENOTRANSPLANTATION, 13, 3, 224, 232,   2006 05 , 10.1111/j.1399-3089.2006.00290.x
    Summary:Background: The induction of xenogeneic hematopoietic chimerism is an attractive approach for overcoming the host response to xenografts, but establishing xenogeneic chimerism requires severe myeloablative conditioning of the recipient. The goal of this study was to determine if co-stimulation blockade would facilitate chimerism and xenograft tolerance in irradiation-conditioned concordant recipients. Methods: Wistar Furth rat bone marrow (BM) cells were injected into irradiation-conditioned C57BL/6 mice with or without co-administration of anti-mouse CD154 monoclonal antibody (mAb). Chimerism was quantified by flow cytometry, and mice were transplanted with WF rat skin and islet xenografts. Results: Blockade of CD40-CD154 interaction facilitated establishment of xenogeneic chimerism in mice conditioned with 600 cGy irradiation. Anti-CD154 mAb was not required for establishment of chimerism in mice treated with 700 cGy. However, mice irradiated with 700 cGy but not treated with anti-CD154 mAb developed a "graft-versus-host disease (GVHD)-like" wasting syndrome and died, irrespective of their development of chimerism. Xenogeneic chimeras established with irradiation and anti-CD154 mAb treatment exhibited prolonged skin and, in many cases, permanent islet xenograft survival. Chimerism was unstable and eventually lost in most recipients. Skin xenografts were rejected even in mice that remained chimeric, whereas most islet xenografts survived to the end of the observation period. Conclusions: Blockade of host CD40-CD154 interaction facilitates the establishment of xenogeneic chimerism and prevents wasting disease and death. Chimerism permits prolonged xenograft survival, but chimerism generated in this way is unstable over time. Skin xenografts are eventually rejected, whereas most islet xenografts survive long term and perhaps permanently.
  • Modification of the anchor residue to MHC class I augments CTL-inducing ability of epitope peptides derived from dengue virus NS3 Protein, Masaki,H, Fujii,Y, Irimajiri,K, Munakata,H, Tomura,T, Kurane,I, Dengue Bulletin, 30, 171,   2006
  • Induction of flavivirus cross-reactive CTLs by immunization with single dengue virus - Derived CTL epitope peptide, H Masaki, Y Fujii, T Tomura, Kurane, I, IMMUNOLOGY 2004: CYTOKINE NETWORK, REGULATORY CELLS, SIGNALING, AND APOPTOSIS, APPENDIX, 115, 121,   2004
    Summary:We investigated whether immunization with the single defined cytotoxic T lymphocyte (CTL) epitope peptide (GYISTRVGM) spanning amino acid (a.a.) residues 299-307 of NS3 of dengue virus types 1 and 3 induces not only the type I and 3 - specific cytotoxic T lymphocytes (CTLs) but also the CTLs cross-reactive to the other type (2 and 4) viruses as well as the related flaviviruses, as is the same with dengue virus infection. The effector CTLs were induced from the draining lymphnode cells of the BALB/c mice (H-2(d)) immunized with the modified epitope peptide (GYISTRVGL) by in vitro stimulation with the same peptide - pulsed syngeneic spleen cells and IL-2. Cytotoxicity was analysed by 4hr Cr-51 release assay using the peptide-pulsed and Cr-51-labeled P815 (H-2(d)) as target cells. The effector cells induced with the modified epitope peptide lysed not only the target cells pulsed with the modified peptide but also those pulsed with the original epitope peptide. These cells were cross-reactive to the peptides spanning a.a. 298-306 (GYISTRVEM) of NS3 of dengue virus types 2 and 4, or the peptide derived from the related flavivirus, such as kunjin virus or Murray Valley encephalitis virus. Cytotoxicity was impaired by substitution at the position 3, 5, or 6, when the epitope peptides with individual substitutions at each residue of the position 3 through 7 were used to pulse the target cells. These results indicate that immunization with single CTL epitope peptide of dengue virus induces not only type-specific CTLs but also the CTLs cross-reactive to the other serotypes as well as the related flaviviruses, and that the a.a. residues at the positions 3(I), 5 (T), and 6 (R) are critical for cross-reactivity.
  • Induction of cytotoxic T lymphocytes by immunization with dengue virus - derived, modified epitope peptide, using dendritic cells as a peptide delivery system, Fujii,Y, Masaki,H, Tomura,T, Irimajiri,K, Kurane,I, Dengue Bulletin, 28, 145,   2004
  • Induction of flavivirus cross-reactive CTLs by immunization with single dengue virus - Derived CTL epitope peptide, H Masaki, Y Fujii, T Tomura, Kurane, I, IMMUNOLOGY 2004: CYTOKINE NETWORK, REGULATORY CELLS, SIGNALING, AND APOPTOSIS, APPENDIX, 115, 121,   2004 , http://www.medimond.com
    Summary:We investigated whether immunization with the single defined cytotoxic T lymphocyte (CTL) epitope peptide (GYISTRVGM) spanning amino acid (a.a.) residues 299-307 of NS3 of dengue virus types 1 and 3 induces not only the type I and 3 - specific cytotoxic T lymphocytes (CTLs) but also the CTLs cross-reactive to the other type (2 and 4) viruses as well as the related flaviviruses, as is the same with dengue virus infection. The effector CTLs were induced from the draining lymphnode cells of the BALB/c mice (H-2(d)) immunized with the modified epitope peptide (GYISTRVGL) by in vitro stimulation with the same peptide - pulsed syngeneic spleen cells and IL-2. Cytotoxicity was analysed by 4hr Cr-51 release assay using the peptide-pulsed and Cr-51-labeled P815 (H-2(d)) as target cells. The effector cells induced with the modified epitope peptide lysed not only the target cells pulsed with the modified peptide but also those pulsed with the original epitope peptide. These cells were cross-reactive to the peptides spanning a.a. 298-306 (GYISTRVEM) of NS3 of dengue virus types 2 and 4, or the peptide derived from the related flavivirus, such as kunjin virus or Murray Valley encephalitis virus. Cytotoxicity was impaired by substitution at the position 3, 5, or 6, when the epitope peptides with individual substitutions at each residue of the position 3 through 7 were used to pulse the target cells. These results indicate that immunization with single CTL epitope peptide of dengue virus induces not only type-specific CTLs but also the CTLs cross-reactive to the other serotypes as well as the related flaviviruses, and that the a.a. residues at the positions 3(I), 5 (T), and 6 (R) are critical for cross-reactivity.
  • Induction of cytotoxic T lymphocytes of heterogeneous specificities by immunization with a single peptide derived from influenza A virus, H Masaki, M Tamura, Kurane, I, VIRAL IMMUNOLOGY, 13, 1, 73, 81,   2000
    Summary:We examined whether immunization with a single peptide induces cytotoxic T lymphocytes (CTLs) of heterogeneous specificities in vivo, Immunization of BALB/c mice with the peptide H2:529-537, which corresponded to amino acid residues 529-537 on the HA2 subunit transmembrane region of influenza A/Jap virus (H2N2) and possessed an H-2K(d)-binding motif, induced CD8(+)CD4(-) CTLs. These CTLs lysed influenza A/Jap virus-infected target cells as well as those pulsed with the H2:529-537 peptide, H2:529-537 peptide-induced CTLs also lysed to lower but significant levels the target cells pulsed with the H1:533-541 peptide, which corresponded to amino acid residues 533-541 on the HA2 subunit transmembrane region of influenza A/PR/8 virus (H1N1) and were compatible to H2:529-537. Immunization with the H1:533-541 peptide, which also possessed an H-2K(d)-binding motif, induced CTLs in vivo, H1:533-541-induced CTLs lysed influenza A/PR/8 virus-infected target cells and those pulsed with the peptide H1:533-541. Subtype cross-reactive CTLs to the H2:529-537 peptide were not induced by immunization with the H1:533-541 peptide, Two peptides, H2:3S and H2:7S, which had one amino acid substitution, serine at the third and seventh positions, respectively, induced CTLs that lysed target cells pulsed with the respective peptides to the highest levels. These results indicate that immunization with a single peptide induces CTLs of heterogeneous specificities in vivo.
  • Definition of an epitope on Japanese encephalitis virus (JEV) envelope protein recognized by JEV-specific murine CD8(+) cytotoxic T lymphocytes, K Takada, H Masaki, E Konishi, M Takahashi, Kurane, I, ARCHIVES OF VIROLOGY, 145, 3, 523, 534,   2000 , 10.1007/s007050050043
    Summary:We defined an epitope on the Japanese encephalitis virus (JEV) envelope (E) protein recognized by CD8(+) cytotoxic T lymphocytes (CTLs). CTLs induced in JEV-infected BALB/c (H-2(d)) mice recognized E and/or premembrane (PrM) proteins, while CTLs in C57BL/6J (H-2(b)) and C3H/HeJ (H-2(k)) mice did not. JEV-specific CTLs had a phenotype of CD3(+) CD4(-) CD8(+). Twenty-four 9-amino acid (a.a.) peptides, which had binding motifs for H-2K(d), H-2L(d) or H-2D(d), were synthesized according to the amino acid sequences of PrM and E proteins. CTLs induced by JEV infection recognized only the peptide K-3. Immunization of BALB/c mice with only a group of peptides including K-3 induced CTLs which recognized the homologous K-3 peptide, while immunization with other peptides did not. The peptide K-3 had a binding motif for H-2K(d). This is consistent with the finding that JEV-specific CTLs in BALB/c mice was H-2K(d)-restricted. These results indicate that the epitope recognized by CTLs in BALB/c mice is located between a.a. 60 and 68 on the E protein, corresponding to an a.a. sequence of CYHASVTDI.
  • Characterization of the I-Ed - restricted peptide recognized by an anti-idiotypic CD4+ T cell line, Masaki,H, Yamane,S, Irimajiri,K, Horiuchi,A, Yamaguchi,J, Suzuki,R, Kurane,I, Journal of Clinical and Laboratory Immunology, 49, 1,   1997
  • Establishment and characterization of an anti-idiotypic CD4(+) CD8(-) T cell line to murine anti-alpha(1->3) dextran antibody, H Masaki, K Irimajiri, A Horiuchi, J Yamaguchi, T Toyosaki, R Suzuki, Kurane, I, CELLULAR IMMUNOLOGY, 174, 2, 180, 189,   1996 12 , 10.1006/cimm.1996.0308
    Summary:It is known that anti-alpha(1 --> 3) dextran antibodies of BALB/c mice are ordinarily of distinctive idiotypes (Id), one of which is the individual idiotype (IdI) that is represented by J558 or M104E to myeloma protein. In the present study, we established T cell line of Th1 type which recognized the Id of anti-alpha(1 --> 3) dextran antibody, and investigated its specificity and functions. The T cell line, named J-2R, had a phenotype of CD3(+) CD4(+) CD8(-) and expressed alpha beta-T cell receptors (TcR). J-2R proliferated in response to J558 in an I-E(d)-restricted manner but did not respond to M104E which had substitution at amino acids 100 and 101. We confirmed that J-2R recognized J558 IdI, using synthetic peptides corresponding to two serial amino acid residues, Arg(100) and Tyr(101), spanning the J558 IdI in the third hypervariable region (hv3) of the heavy chain. alpha(1 --> 3) dextran-binding B cells which were isolated from dextran-immunized mice activated J-2R, but B cells from nonimmune mice did not. J-2R produced IL-2, IFN-gamma and IL-6, but did not produce IL-4, IL-5, or IL-10. Furthermore, J-2R inhibited the growth of J558 myeloma cells inoculated to the syngeneic mice in vivo. These findings suggest that Id-specific CD4(+) T cells, J-2R, are involved in Id network and may play a role in vivo. J-2R is useful for analysis of the role of the Id-specific helper T cells in immune network because J558 IdI is frequently present on anti-alpha(1 --> 3) dextran antibodies. (C) 1996 Academic Press, Inc.
  • DETECTION OF MINIMAL RESIDUAL DISEASE USING CLONOSPECIFIC PRIMERS FOR CDRIII IN PATIENTS WITH ACUTE B-LYMPHOCYTIC-LEUKEMIA WITH OR WITHOUT PHILADELPHIA-CHROMOSOME - POSSIBILITY OF CLINICAL-APPLICATION AS A TOOL FOR IMPROVING PROGNOSIS, Y MAEDA, F HORIUCHI, S MORITA, M MATSUDA, C SHIRAKAWA, H MASAKI, A KOYAMA, H HAMAZAKI, T FUJIMOTO, K IRIMAJIRI, A HORIUCHI, EXPERIMENTAL HEMATOLOGY, 22, 9, 881, 887,   1994 08
    Summary:We attempted to identify the minimal residual leukemic clone as related to the clinical course in patients with acute B lymphocytic leukemia (B-ALL). DNA was extracted from stored bone marrow slides, and the third complementarity determining region (CDRIII) was amplified by polymerase chain reaction (PCR) using primers with consensus sequences for V-H and J(H). After amplification of the CDRIII band, the DNA fragment of CDRIII was inserted into the cloning vector PUC118. After cloning, the DNA sequences for CDRIII were determined. Clonospecific DNA sequences in CDRIII were selected, and clonospecific primers for each patient were synthesized. Using the clonospecific primers, we carried out second-round PCR to detect minimal residual disease (MRD) during several stages of the clinical course. Basically, the sensitivity of detection for MRD was between 10(-4) and 10(-5) cells. Even when leukemic cells were not detected in the morphologic study, with this detection system, the MRD was identified as an amplified CDRIII band stained with ethidium bromide on agarose gel. After bone marrow transplantation (BMT), MRD was detected for at least 4 months. In this article, we discuss the difference in sensitivity of detection for MRD between the BCR-ABL fusion gene and CDRIII in Philadelphia chromosome-positive (Ph(+)) B-ALL, as well as the possible clinical application of this method to predict relapse and prognosis.
  • CD3 DOWN-REGULATING FACTOR IN SERA AND CULTURE SUPERNATANTS OF LEUKEMIC-CELLS FROM PATIENTS WITH ADULT T-CELL LEUKEMIA, M MATSUDA, Y MAEDA, C SHIRAKAWA, H MASAKI, A KOYAMA, F HORIUCHI, H HAMAZAKI, T FUJIMOTO, K IRIMAJIRI, A HORIUCHI, BRITISH JOURNAL OF HAEMATOLOGY, 83, 2, 212, 217,   1993 02
    Summary:Immunological abnormality of T lymphocytes in patients with adult T cell leukaemia (ATL) is characterized by abnormal expression of the 55 kD chain of the receptor for interleukin 2 (IL-2R/p55) (Tac), and the down-regulation of CD3 expression. Using serum and culture supernatants of leukaemic cells from ATL patients (Group A) whose CD3 expression was down-regulated and those (Group B) whose CD3 was not low, the possible mechanism of CD3 down-regulation on ATL cells was discussed. When PBMC from normal individuals were cultured with sera from ATL patients for 24 h, CD3 expression revealed by mean fluorescent intensity (MFI) was down-regulated by sera from ATL patients in Group A (MFI: Pt 1=51.6+/-4.5, Pt 2=48.0+/-6.9, control=96.5+/-6.6), not by sera from patients in Group B (MFI: Pt 3=105.5+/-7.9, Pt 4=102.5+/-8.3, control=96.5+/-6.6).When normal PBMC were cultured with supernatants of leukaemic cells from ATL patients in Group A, this CD3 down-regulating activity was also detected (MFI: Pt 1=78.0+/-10.2, Pt 2=70.6+/-8.7, control=94.0+/-6.6). By using gel-chromatography, the fractionated supernatants from ATL patients in Group A decreased CD3 expression of normal PBMC significantly (MFI: Pt 1=22.9+/-5.8, Pt 2=28.8+/-7.4, control=92.1+/-9.6). This CD3 down-regulating activity in fractionated supernatant was not inhibited by any lymphokine antibodies, anti-IL-1alpha antibody (Ab), anti-IL-1B Ab, anti-IL-2 Ab, anti-IL-3 Ab, anti-IL-4 Ab, anti-IL-6 Ab, anti-TNF-alpha Ab and anti-IFN-gamma Ab. Any known cytokines (IL-1, IL-2, IL-3, IL-4, IL-6, TNF-alpha and IFN-gamma) could not modulate CD3 expression of normal PBMC. These findings suggested that there are novel factor(s) with CD3 down-regulating activity in the serum and culture supernatant of ATL patient and those factor(s) are involved in progression of ATL.
  • GENERATION OF HELPER T-CELLS THAT RECOGNIZE A CROSS-REACTIVE IDIOTYPE THROUGH A NETWORK MECHANISM, H MASAKI, K IRIMAJIRI, MICROBIOLOGY AND IMMUNOLOGY, 36, 3, 279, 295,   1992
    Summary:T cells that recognize the cross-reactive idiotype expressed on the heavy (H) chain of M104E (IgM, lambda(1)) were induced in BALB/c mice by immunization with Dextran B-1355. T cells derived from mice immunized with 1 mg of Dextran B-1355 showed a marked proliferative response against M104E, whereas T cells from mice immunized with Ficoll or lesser amounts of Dextran B-1355 did not. BCL1Id, which had an immunoglobulin isotype identical to M104E, did not induce proliferation of the T cells. These T cells also proliferated against J558 (IgA, lambda(1)) which shared the cross-reactive idiotype of the anti-alpha (1 --> 3) glucosidic linkage antibody with M104E on the H chain. The T cells proliferated more efficiently against F(ab')2-104E. Fab-104E and H104E, the H chain of M104E, than against intact M104E. The T cell proliferative response against the idiotype on M104E or even H104E required macrophages as antigen-presenting cells (APC) and the response was inhibited when APC were treated with NH4Cl or chloroquine, inhibitors of antigen processing. Moreover, anti-CD4 antibody or anti-Ia antibody inhibited the proliferative response. These results indicated that anti-idiotypic T cells of the helper type, which recognized a cross-reactive idiotype associated with Ia molecules in processed form, could be induced physiologically through a network mechanism.
  • INDUCTION OF ANTIIDIOTYPIC T-CELLS THROUGH A NETWORK MECHANISM, H MASAKI, C SHIRAKAWA, M MATSUDA, S MORITA, A KOYAMA, F HORIUCHI, H HAMAZAKI, T FUJIMOTO, Y MAEDA, K IRIMAJIRI, A HORIUCHI, IMMUNOLOGY LETTERS, 30, 1, 107, 112,   1991 09
    Summary:BALB/c mouse T cells that recognized the idiotype expressed on M104E(mu, lambda-1) were induced by immunization with Dextran B-1355. T cells derived from mice immunized with 1 mg of Dextran B-1355 showed a marked proliferative response against M104E, whereas T cells from mice immunized with Ficoll or smaller amounts of Dextran B-1355 did not. BCL1Id, which had an identical isotype, did not induce proliferation of T cells. The T cell proliferative response against the idiotype on M104E required macrophages as antigen-presenting cells. The proliferative response was inhibited when antigen-presenting cells were treated with NH4Cl or chloroquine, which are antigen-processing inhibitors. These results indicate that anti-idiotypic T cells which recognized processed idiotopes could be induced physiologically through a network mechanism.

Awards & Honors

  •   1997 , Kinki University Medical Association Award

Research Grants & Projects

  • Juvenile Diabetes Foundation, Juvenile Diabetes Foundation International Research Award, Autoreactive T cell clone in BB rats
  • Grant-in-Aid for Scientific Research, Fundamental research for development of CTL-inducible vaccine against West Nile virus infection using recombinant E protein
  • Induction of dengue virus - specific cytotoxic T lymphocytes by peptide immunization
  • Induction of influenza virus - specific cytotoxic T lymphocytes by peptide immunization
  • Establishment of idiotype-specific helper T cell line and analysis of its effects to immune network