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今井 優樹イマイ マサキ

所属部署医学研究科免疫学分野
職名講師
メールアドレスimaimmed.nagoya-cu.ac.jp
ホームページURL
生年月日
Last Updated :2019/04/20

研究者基本情報

学位

  • 名古屋市立大学/博士(医学)

研究活動情報

研究キーワード

    補体, 抗体, 腫瘍免疫

論文

  • Regulatory T cells expressing abundant CTLA-4 on the cell surface with a proliferative gene profile are key features of human head and neck cancer., Matoba T, Imai M, Ohkura N, Kawakita D, Ijichi K, Toyama T, Morita A, Murakami S, Sakaguchi S, Yamazaki S, International journal of cancer,   2018年11月, 査読有り
  • Complement component 5 promotes lethal thrombosis., Mizuno T, Yoshioka K, Mizuno M, Shimizu M, Nagano F, Okuda T, Tsuboi N, Maruyama S, Nagamatsu T, Imai M., Sci Rep, 7,   2017年02月, 査読有り
  • Ultraviolet B-Induced Maturation of CD11b-Type Langerin- Dendritic Cells Controls the Expansion of Foxp3+ Regulatory T Cells in the Skin., Yamazaki S, Odanaka M, Nishioka A, Kasuya S, Shime H, Hemmi H, Imai M, Riethmacher D, Kaisho T, Ohkura N, Sakaguchi S, Morita A, Journal of immunology (Baltimore, Md. : 1950), 200, (1) 119 - 129,   2018年01月, 査読有り
  • C5a inhibitor protects against ischemia/reperfusion injury in rat small intestine., Tuboly E, Futakuchi M, Varga G, Érces D, Tőkés T, Mészáros A, Kaszaki J, Suzui M, Imai M, Okada A, Okada N, Boros M, Okada H., Microbiol Immunol., 60, (1) 35 - 46,   2016年01月, 査読有り
  • Expression of membrane complement regulators, CD46, CD55 and CD59, in mesothelial cells of patients on peritoneal dialysis therapy., Sei Y, Mizuno M, Suzuki Y, Imai M, Higashide K, Harris CL, Sakata F, Iguchi D, Fujiwara M, Kodera Y, Maruyama S, Matsuo S, Ito Y., Molecular immunology, 65, (2) 302 - 309,   2015年06月, 査読有り
  • Anti-C5a complementary peptide ameliorates acute peritoneal injury induced by neutralization of Crry and CD59., Mizuno T, Mizuno M, Imai M, Suzuki Y, Kushida M, Noda Y, Maruyama S, Okada H, Okada N, Matsuo S, Ito Y, American journal of physiology. Renal physiology, 305, (11) F1603 - 16,   2013年12月, 査読有り
  • Inflammatory Activation after Experimental Cardiac Tamponade., Vass A, Süveges G, Erces D, Nógrády M, Varga G, Földesi I, Futakuchi M, Imai M, Okada N, Okada H, Boros M, Kaszaki J, Eur Surg Res, 51, 1 - 13,   2013年, 査読有り
  • Anti-C5a complementary peptide ameliorates acute peritoneal injuries induced by neutralization of Crry and CD59., Mizuno T, Mizuno M, Imai M, Suzuki Y, Kushida M, Noda Y, Maruyama S, Okada H, Okada N, Matsuo S, Ito Y., Am J Physiol Renal Physiol,, 305, F1603 - 1616,   2013年, 査読有り
  • Interleukin-17A-Producing T Lymphocytes in Chronic Active Epstein-Barr Virus Infection., Ohta R, Imai M, Kawada J, Kimura H, Ito Y, Microbiol. Immunol., 57, (2) 139 - 144,   2013年02月, 査読有り
  • Complement C5A Antagonist Treatment Improves the Acute Circulatory and Inflammatory Consequences of Experimental Cardiac Tamponade., Erces D, Nógrády M, Nagy E, Varga G, Vass A, Süveges G, Imai M, Okada N, Okada H, Boros M, Kaszaki J., Crit Care Med, 41, e344 - 351,   2013年, 査読有り
  • Serum concentrations of complement anaphylatoxins and proinflammatory mediators in patients with 2009 H1N1 influenza., Ohta R, Torii Y, Imai M, Kimura H, Okada N, Ito Y, Microbiol. Immunol., 55, (3) 191 - 198,   2011年03月, 査読有り
  • Novel Complementary Peptides to Target Molecules., Okada H, Imai M, Ono F, Okada A, Tada T, Mizue Y, Terao K, Okada N, Anticancer Res, 31, (7) 2511 - 2516,   2011年07月, 査読有り
  • Endothelin receptor antagonist attenuates oxidative stress in a neonatal sepsis piglet model., Goto T, Hussein MH, Kato S, Daoud GA, Kato T, Sugiura T, Kakita H, Nobata M, Kamei M, Mizuno H, Imai M, Ito T, Kato I, Suzuki S, Okada N, Togari H, Okada H, Pediatric research, 72, (6) 600 - 605,   2012年12月, 査読有り
  • Increased levels of cytokines and high-mobility group box 1 are associated with the development of severe pneumonia, but not acute encephalopathy, in 2009 H1N1 influenza-infected children., Ito Y, Torii Y, Ohta R, Imai M, Hara S, Kawano Y, Matsubayashi T, Inui A, Yoshikawa T, Nishimura N, Ozaki T, Morishima T, Kimura H, Cytokine, 56, (2) 180 - 187,   2011年11月, 査読有り
  • Endothelin Receptor Antagonist Attenuates Oxidative Stress in Neonatal Sepsis Model., Goto T, Hussein MH, Kato S, Daoud GA, Kato T, Sugiura T, Kakita H, Nobata M, Kamei M, Mizuno H, Imai M, Ito T, Kato I, Suzuki S, Okada N, Togari H, Okada H, Pediatric Research, 72, 600 - 605,   2012年, 査読有り
  • Endothelin receptor antagonist attenuates inflammatory response and prolongs the survival time in a neonatal sepsis model., Goto T, Hussein MH, Kato S, Daoud GA, Kato T, Sugiura T, Kakita H, Nobata M, Mizuno H, Imai M, Ito T, Kato I, Suzuki S, Okada N, Togari H, Okada H, Eur J Intensive Care Med., 36, (12) 2132 - 2139,   2010年12月, 査読有り
  • Effects of active and inactive phospholipase D2 on signal transduction, adhesion, migration, invasion, and metastasis in EL4 lymphoma cells., Knoepp SM, Chahal MS, Xie Y, Zhang Z, Brauner DJ, Hallman MA, Robinson SA, Han S, Imai M, Tomlinson S, Meier KE.今井 優樹, Mol Pharmacol., 74, (3) 574 - 584,   2008年09月, 査読有り
  • Connective tissue growth factor (CTGF/CCN2) is increased in peritoneal dialysis patients with high peritoneal solute transport rate., Mizutani M, Ito Y, Mizuno M, Nishimura H, Suzuki Y, Hattori R, Matsukawa Y, Imai M, Oliver N, Goldschmeding R, Aten J, Krediet RT, Yuzawa Y, Matsuo S, Am J Physiol Renal Physiol., 298, F721 - 733,   2010年, 査読有り
  • Modulation of protective T cell immunity by complement inhibitor expression on tumor cells., Varela JC, Imai M, Atkinson C, Ohta R, Rapisardo M, Tomlinson S,, Cancer Res., 68, (16) 6734 - 6742,   2008年08月, 査読有り
  • Procarboxypeptidase R Deficiency Causes Increased Lethality in Concanavalin A -induced Hepatitis in Female Mice., Asai S, Kimbara N, Tada T, Imai M*, Campbell W, Okada H, OkadaN, Biol Pharm Bull, 33, 1256 - 1259,   2010年, 査読有り
  • Effect of the antibody immunotherapy by the anti-MUC1 monoclonal antibody to the oral squamous cell carcinoma in vitro., Shimizu M, Imai M, Biological & pharmaceutical bulletin, 31, (12) 2288 - 2293,   2008年12月, 査読有り
  • ffect of the antibody immunotherapy by the anti-MUC1 monoclonal antibody to the oral squamous cell carcinoma in vitro., Shimizu M, Imai M, Biol Pharm Bull, 31, 2288 - 2293,   2008年, 査読有り
  • Enhancement of antibody-dependent mechanisms of tumor cell lysis by a targeted activator of complement., Imai M, Ohta R, Varela JC, Song H, Tomlinson S, Cancer research, 67, (19) 9535 - 9541,   2007年10月, 査読有り
  • Inhibition of HIV-1 infection by synthetic peptides derived CCR5 fragments., Imai M, Baranyi L, Okada N, Okada H, Biochemical and biophysical research communications, 353, (4) 851 - 856,   2007年02月, 査読有り
  • Complement-mediated mechanisms in anti-GD2 monoclonal antibody therapy of murine metastatic cancer., Imai M, Landen C, Ohta R, Cheung NK, Tomlinson S, Cancer research, 65, (22) 10562 - 10568,   2005年11月, 査読有り
  • Complement inhibitors targeted to the proximal tubule prevent injury in experimental nephrotic syndrome and demonstrate a key role for C5b-9., He C, Imai M, Song H, Quigg RJ, Tomlinson S, Journal of immunology (Baltimore, Md. : 1950), 174, (9) 5750 - 5757,   2005年05月, 査読有り
  • Inhibition of HIV-1 infection in cells expressing an artificial complementary peptide., Hosokawa M, Imai M, Okada H, Okada N, Biochemical and biophysical research communications, 324, (1) 236 - 240,   2004年11月, 査読有り
  • Inhibition of a complement regulator in vivo enhances antibody therapy in a model of mammary adenocarcinoma., Imai M, Ohta R, Okada N, Tomlinson S, International journal of cancer, 110, (6) 875 - 881,   2004年07月, 査読有り
  • Mouse complement receptor-related gene y/p65-neutralized tumor vaccine induces antitumor activity in vivo., Ohta R, Kondor N, Dohi N, Tomlinson S, Imai M, Holers VM, Okada H, Okada N, Journal of immunology (Baltimore, Md. : 1950), 173, (1) 205 - 213,   2004年07月, 査読有り
  • The effect of dexamethasone on human mucin 1 expression and antibody-dependent complement sensitivity in a prostate cancer cell line in vitro and in vivo., Imai M, Hwang HY, Norris JS, Tomlinson S, Immunology, 111, (3) 291 - 297,   2004年03月, 査読有り
  • Expression of rat complement control protein Crry on tumor cells inhibits rat natural killer cell-mediated cytotoxicity., Caragine TA, Imai M, Frey AB, Tomlinson S, Blood, 100, (9) 3304 - 3310,   2002年11月, 査読有り
  • CD59 blocks not only the insertion of C9 into MAC but inhibits ion channel formation by homologous C5b-8 as well as C5b-9, Imre Farkas, Imre Farkas, Lajos Baranyi, Lajos Baranyi, Yasushige Ishikawa, Noriko Okada, Csaba Bohata, Denes Budai, Atsuo Fukuda, Masaki Imai, Hidechika Okada, Hidechika Okada, Journal of Physiology, 539, 537 - 545,   2002年03月01日, Activation of the complement system on the cell surface results in the insertion of pore forming membrane attack complexes (MAC, C5b-9). In order to protect themselves from the complement attack, the cells express several regulatory molecules, including the terminal complex regulator CD59 that inhibits assembly of the large MACs by inhibiting the insertion of additional C9 molecules into the C5b-9 complex. Using the whole cell patch clamp method, we were able to measure accumulation of homologous MACs in the membrane of CD59-human B-cells, which formed non-selective ion channels with a total conductance of 360 ± 24 pS as measured at the beginning of the steady-state phase of the inward currents. C5b-8 and small-size MAC (MAC containing only a single C9) can also form ion channels. Nevertheless, in CD59+human B-cells in spite of small-size MAC formation, an ion current could not be detected. In addition, restoring CD59 to the membrane of the CD59-cells inhibited the serum-evoked inward current. The ion channels formed by the small-size MAC were therefore sealed, indicating that CD59 directly interfered with the pore formation of C5b-8 as well as that of small-size C5b-9. These results offer an explanation as to why CD59-expressing cells are not leaky in spite of a buildup of homologous C5b-8 and small-size MAC. Our experiments also confirmed that ion channel inhibition by CD59 is subject to homologous restriction and that CD59 cannot block the conductivity of MAC when generated by xenogenic (rabbit) serum.
  • Inhibition of HIV-1 infection by an intramolecular antisense peptide to T20 in gp160, Masaki Imai, Noriko Okada, Hidechika Okada, Hidechika Okada, Microbiology and Immunology, 44, 205 - 212,   2000年01月01日, Antisense amino acids are amine acids which can be translated from the corresponding anti-codons of a sense amino acid. Antisense peptides encoded by the noncoding DNA strand have a tendency to interact with each other. We have demonstrated that antisense peptide sequences are present intramolecularly, and these may contribute to the folding and maintenance of the tertiary structure of a protein. T20 is a synthetic peptide with an amino acid sequence in the gp41 of HIV-1 and has been demonstrated to be a potent inhibitor of HIV-1 infection. We searched for intramolecular peptide sequences which are antisense to portions of T20. A synthetic peptide (TA-1L) consisting of amino acids 84 to 97 of gp160, which contains an antisense peptide sequence (TA-1) to T20, was shown to inhibit HIV-1(IIIB) infection of MT-4 cells. Interaction of these antisense peptides could be involved in sustaining HIV-1 infectivity. The TA-1L site, which exists in the C1 domain of gp160, is highly homologous among strains of HIV-1, especially at TA-1 and in the amino acids flanking the C terminus. Although the TA-1 sites of 18 out of 30 HIV-1 strains were antisense to the T20 region, those of the remaining 12 strains, including HIV-1(MN), were not. However, TA-1L inhibited infection by HIV-1(MN), which has no antisense peptide in T20 corresponding to TA-1, although the inhibitory effect was weaker. TA-1L may thus also interfere with the gp160 interaction with CD4, which has an antisense sequence to TA-1.
  • Characterization of mouse DAF on transfectant cells using monoclonal antibodies which recognize different epitopes, Rieko Ohta, Masaki Imai, Yoshihiro Fukuoka, Takashi Miwa, Noriko Okada, Hidechika Okada, Hidechika Okada, Microbiology and Immunology, 43, 1045 - 1056,   1999年01月01日, Several membrane proteins prevent host cells from homologous complement attack. In humans, one such protein, decay-accelerating factor (DAF), exists as two isoforms, a GPI anchored form and a secreted form, which are generated by alternative splicing. DAF in mouse is also expressed as two isoforms, a GPI anchored form (GPI-DAF) and a transmembrane form (TM-DAF), which are produced from two separate genes. In this study, we transfected cDNA of mouse GPI-DAF or TM-DAF into Chinese hamster ovary (CHO) cells. Both isoforms of DAF on CHO cells were shown to regulate mouse complement C3 deposition mediated by the classical and alternative pathways and the inhibitory activity of both isoforms was species restricted. The two mouse DAF isoforms were effective against rat complement but not against human and guinea pig complement. Furthermore, we produced hamster mAbs to mouse DAF using GPI-DAF transfectant cells and established seven unique mAbs (RIKO-1-7). Western blotting analysis using RIKO-3, which reacts with both GPI-DAF and TM-DAF, and RIKO-4, which is an anti-GPI-DAF specific mAb, indicated that GPI-DAF was expressed on erythrocytes, spleen and testis, and that TM-DAF was expressed only in testis.

書籍等出版物

  • 補体への招待, メジカルビュー社,   2011年


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