Search

Your search keyword '"Masuko, Kazutaka"' showing total 20 results
Start Over Author "Masuko, Kazutaka"
20 results on '"Masuko, Kazutaka"'

5. Contributors

Author

Andoniou, Christopher E., primary, Balato, Anna, additional, Basse, Per H., additional, Bekiaris, Vasileios, additional, Bernardini, Giovanni, additional, Briercheck, Edward L., additional, Bryan, Maryanne A., additional, Butterfield, Lisa H., additional, Cahalan, Michael D., additional, Caligiuri, Michael A., additional, Camp, William L., additional, Carlino, Claudia, additional, Carlyle, James R., additional, Carrega, Paolo, additional, Chambers, Benedict J., additional, Chamoto, Kenji, additional, Cooley, Sarah, additional, Costello, Régis, additional, Coudert, Jerome D., additional, Daldrup-Link, Heike, additional, de Armas, Lesley R., additional, Degli-Esposti, Mariapia, additional, Djeu, Julie Y., additional, Epling-Burnette, P.K., additional, Fan, Jia, additional, Fauriat, Cyril, additional, Ferlazzo, Guido, additional, Freud, Aharon G., additional, Garrod, Kym R., additional, Gaspari, Anthony A., additional, Getz, Godfrey S., additional, Gismondi, Angela, additional, Goding, Stephen R., additional, González, Segundo, additional, Goodier, Martin R., additional, Grzywacz, Bartosz, additional, Höglund, Petter, additional, Hosmalin, Anne, additional, Housseau, Franck, additional, Ikeda, Takayuki, additional, Ito, Taisuke, additional, Jha, Priyanka, additional, Kähäri, Veli-Matti, additional, Kanto, Tatsuya, additional, Karlsson-Parra, Alex, additional, Kiessling, Rolf, additional, Klingemann, Hans, additional, Knopp, Christiane, additional, Koizumi, Shinichi, additional, Komoriya, Akira, additional, Kuo, Ming-Ling, additional, Lane, Peter J.L., additional, Lee, Yen-Chang, additional, Liippo, Jussi, additional, Lin, Syh-Jae, additional, Liu, Siyuan, additional, Ljunggren, Hans-Gustaf, additional, López-Larrea, Carlos, additional, López-Soto, Alejandro, additional, Lotze, Michael T., additional, Loux, Tara J., additional, Lu, Lina, additional, Magee, Michael, additional, Mailliard, Robbie B., additional, Male, Victoria H., additional, Mandelboim, Ofer, additional, Masuko, Kazutaka, additional, Matta, Benjamin M., additional, Mavilio, Domenico, additional, Mehrad, Borna, additional, Miller, Jeffery S., additional, Mitamura, Rieko, additional, Moffett, Ashley, additional, Montalto, Erika, additional, Moretta, Alessandro, additional, Moretta, Lorenzo, additional, Morice, William G., additional, Münz, Christian, additional, Nalesnik, Michael A., additional, Niederkorn, Jerry Y., additional, Nishimura, Takashi, additional, Norris, Karen A., additional, Olive, Daniel, additional, Ortaldo, John R., additional, Packard, Beverly Z., additional, Paus, Ralf, additional, Podack, Eckhard R., additional, Qian, Shiguang, additional, Qiu, Shuang-Jian, additional, Ransohoff, Richard M., additional, Reardon, Catherine A., additional, Reinhart, Verena, additional, Rey, Jérôme, additional, Rubartelli, Anna, additional, Santoni, Angela, additional, Scott-Algara, Daniel, additional, Semino, Claudia, additional, Shi, Fu-Dong, additional, Stabile, Helena, additional, Stern-Ginossar, Noam, additional, Subleski, Jeff, additional, Thomson, Angus W., additional, Toriseva, Mervi, additional, Ucker, David S., additional, Velardi, Andrea, additional, Verneris, Michael R., additional, Vujanovic, Lazar N., additional, Vujanovic, Nikola L., additional, Wakita, Daiko, additional, Wei, Sheng, additional, Weiss, Jonathan M., additional, Wels, Winfried S., additional, Wendland, Michael F., additional, Wesa, Amy K., additional, Wiltrout, Robert H., additional, Xiao, Yong-Sheng, additional, Yan, Dah-Chin, additional, Yawata, Makato, additional, Yawata, Nobuyo, additional, Zhang, Alexandra Y., additional, and Zúñiga-Pflücker, Juan Carlos, additional

Published
2010
Full Text
View/download PDF

6. Interaction of NK cells with bacteria

Author

Chamoto, Kenji, primary, Wakita, Daiko, additional, Koizumi, Shinichi, additional, Masuko, Kazutaka, additional, Ikeda, Takayuki, additional, Mitamura, Rieko, additional, and Nishimura, Takashi, additional

Published
2010
Full Text
View/download PDF

7. 一次免疫応答におけるNeuronal leucine-rich repeat protein 3(NLRR3)の機能的役割

Author

Ito, Kyoko, Masuko, Kazutaka, and Ito, Koichi

Subjects
integrin, 神経関連ロイシンリッチリピートタンパク質, 基礎医学, 接着分子, dendritic cells, インテグリン, RGD motif, RGD モチーフ, neuronal leucine-rich repeat protein, 樹状細胞, adhesion molecule
Abstract

Contact between dendritic cells（ DCs） and resting T cells is essential for initiation of the primary immune response. In this study, we examined whether neuronal leucine-rich repeat protein 3 （NLRR3）, a receptor involved in nerve system development, participates in DC-T cell binding and T-cell activation. We confirmed that NLRR3 is expressed on naive T cells. NLRR3 contains an Arg-Gly-Asp （RGD） motif in its amino acid sequence, for which several integrins can be considered as potential ligands. Indeed, monocyte-derived DCs expressed several integrins that can bind to the RGD motif. Functionally, DC-induced resting allogeneic T-cell proliferation was partially inhibited by addition of integrin-specific antibodies and synthetic RGD peptides, indicating that RGD-containing molecules, including NLRR3 and several integrins, at least participate in the events of the initial primary immune response involving naive T cells and DCs. Furthermore, DCs were shown to bind directly to NLRR3-transfected Chinese hamster ovary cells in a NLRR3-dependent manner, and the binding was removed in the presence of integrin-specifi c antibodies. These data suggest that NLRR3 plays an important role in initiation of the primary immune response., 弘前医学. 61(1), 2010, p.46-57

Published
2010

13. Abstract 3615: IL-6/STAT3-dependent immunosuppressive function of tumor-infiltrating dendritic cells in colorectal cancer

Author

Ono, Yosuke, primary, Ohtake, Jyunya, additional, Kaneumi, Shun, additional, Masuko, Kazutaka, additional, Sumida, Kentaro, additional, Kishikawa, Takuto, additional, Terada, Satoshi, additional, Kita, Toshiyuki, additional, Takahashi, Norihiko, additional, Taketomi, Akinobu, additional, and Kitamura, Hidemitsu, additional

Published
2014
Full Text
View/download PDF

16. Activation of IL-6/STAT3-signaling cascade induces suppression of antigen presentation by human dendritic cells (TUM4P.917)

Author

Kitamura, Hidemitsu, primary, Ohno, Yousuke, additional, Ohtake, Junya, additional, Kaneumi, Shun, additional, Kishikawa, Takuto, additional, Terada, Satoshi, additional, Sumida, Kentaro, additional, Masuko, Kazutaka, additional, Kita, Toshiyuki, additional, Takahashi, Norihiko, additional, and Taketomi, Akinobu, additional

Published
2014
Full Text
View/download PDF

19. Anti- IL-6 receptor m Ab eliminates myeloid-derived suppressor cells and inhibits tumor growth by enhancing T-cell responses.

Author

Sumida, Kentaro, Wakita, Daiko, Narita, Yoshinori, Masuko, Kazutaka, Terada, Satoshi, Watanabe, Kazue, Satoh, Takayuki, Kitamura, Hidemitsu, and Nishimura, Takashi

Abstract

CD11b+ Gr-1+ immature myeloid cells ( Im Cs), which are abnormally increased in tumor-bearing mice, were classified into three different subsets according to their phenotypic and morphological characteristics: Gr-1low F4/80+ macrophages ( MΦ- Im Cs), Gr-1mid stab neutrophils ( Neutstab- Im Cs), and Gr-1high segmented neutrophils ( Neutseg- Im Cs). In the spleen, only MΦ- Im Cs but not Neutstab- Im Cs and Neutseg- Im Cs exhibited a significant immunosuppressive activity in MLR. In contrast, tumor-infiltrating leukocytes ( TILs) contained only two Im C subsets, MΦ- Im Cs and Neutseg- Im C, both of which exhibited stronger inhibitory activity against T cells compared with spleen- MΦ- Im Cs. Thus, we concluded that tumor-infiltrating MΦ- Im Cs and Neutseg- Im Cs were fully differentiated myeloid-derived suppressor cells ( MDSCs) with stronger T-cell inhibitory activity. Indeed, spleen MΦ- Im Cs were converted into stronger MΦ- MDSCs by tumor-derived factor ( TDF). Moreover, both spleen Neutstab- Im Cs and Neutseg- Im Cs differentiated into Neutseg- MDSCs with suppressive activity after culture with TDF. We first demonstrated that administration of anti- IL-6 R m Ab could downregulate the accumulation of MΦ- MDSCs and Neutseg- MDSCs in tumor-bearing mice. The elimination of those MDSCs caused subsequent enhancement of antitumor T-cell responses, including IFN-γ-production. The therapeutic effect of anti- IL-6 R m Ab was further enhanced by combination with gemcitabine ( GEM). Thus, we propose that anti- IL-6 R m Ab could become a novel tool for the downmodulation of MDSCs to enhance antitumor T-cell responses in tumor-bearing hosts. [ABSTRACT FROM AUTHOR]

Published
2012
Full Text
View/download PDF

20. The Key Role of IL-6-Arginase Cascade for Inducing Dendritic Cell-Dependent CD4+ T Cell Dysfunction in Tumor-Bearing Mice.

Author

Narita, Yoshinori, Kitamura, Hidemitsu, Wakita, Daiko, Sumida, Kentaro, Masuko, Kazutaka, Terada, Satoshi, Nakano, Kiichiroh, and Nishimura, Takashi

Subjects
*INTERLEUKIN-6, *ARGINASE, *DENDRITIC cells, *CD4 antigen, *T cells, *LABORATORY mice, *TUMOR immunology
Abstract

Evaluation of immune dysfunction during the tumor-bearing state is a critical issue in combating cancer. In this study, we initially found that IL-6, one of the cachectic factors, suppressed CD4+ T cell-mediated immunity through downregulation of MHC class II by enhanced arginase activity of dendritic cells (DC) in tumor-bearing mice. We demonstrated that administration of Ab against IL-6R (anti-IL-6R mAb) greatly enhanced T cell responses and inhibited the growth of tumor in vivo. We also found that IL-6 upregulated the expression of arginase-1 and arginase activity of DC in vitro. Tumor-infiltrating CDllc+ DC exhibited upregu-lated mRNA expression of arginase-1 but reduced expression of MHC class II in parallel with the increase in serum IL-6 levels at the late stage in tumor-bearing hosts. However, the administration of anti-IL-6R mAb into tumor-bearing mice inhibited both the downmodulation of MHC class II and the upregulation of arginase-1 mRNA levels in DC. Furthermore, we noted that Nω-hydroxy-L-arginine or L-arginine, an arginase-1 inhibitor, blocked the reduction in MHC class II levels on CDllc+ DC during the tumor-bearing state. Finally, we demonstrated that the administration of Nω-hydroxy-L-arginine at the peritumor site significantly enhanced CD4+ T cell responses and inhibited tumor growth. Thus, IL-6-mediated arginase activation and the subsequent reduc-tion in MHC class II expression on DC appeared to be critical mechanisms for inducing dysfunction of the immune system in the tumor-bearing state. Blockade of the IL-6-arginase cascade is a promising tool to overcome the dysfunction of antitumor immunity in tumor-bearing hosts. [ABSTRACT FROM AUTHOR]

Published
2013
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results