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3. Fibroblast growth factor 18 stimulates the proliferation of hepatic stellate cells, thereby inducing liver fibrosis

Author

Tsuchiya, Yuichi, Seki, Takao, Kobayashi, Kenta, Komazawa-Sakon, Sachiko, Shichino, Shigeyuki, Nishina, Takashi, Fukuhara, Kyoko, Ikejima, Kenichi, Nagai, Hidenari, Igarashi, Yoshinori, Ueha, Satoshi, Oikawa, Akira, Tsurusaki, Shinya, Yamazaki, Soh, Nishiyama, Chiharu, Mikami, Tetuo, Yagita, Hideo, Okumura, Ko, Kido, Taketomo, Miyajima, Atsushi, Matsushima, Kouji, Imasaka, Mai, Araki, Kimi, Imamura, Toru, Ohmuraya, Masaki, Tanaka, Minoru, and Nakano, Hiroyasu

Published
2023
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4. cFLIP suppression and DR5 activation sensitize senescent cancer cells to senolysis

Author

Wang, Liqin, Jin, Haojie, Jochems, Fleur, Wang, Siying, Lieftink, Cor, Martinez, Isabel Mora, De Conti, Giulia, Edwards, Finn, de Oliveira, Rodrigo Leite, Schepers, Arnout, Zhou, Yangyang, Zheng, Jiaojiao, Wu, Wei, Zheng, Xingling, Yuan, Shengxian, Ling, Jing, Jastrzebski, Kathy, Santos Dias, Matheus Dos, Song, Ji-Ying, Celie, Patrick N. H., Yagita, Hideo, Yao, Ming, Zhou, Weiping, Beijersbergen, Roderick L., Qin, Wenxin, and Bernards, René

Published
2022
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9. Anti-CD80/86 antibodies inhibit inflammatory reaction and improve graft survival in a high-risk murine corneal transplantation rejection model

Author

Zhu, Jun, Inomata, Takenori, Nakamura, Masahiro, Fujimoto, Keiichi, Akasaki, Yasutsugu, Fujio, Kenta, Yanagawa, Ai, Uchida, Koichiro, Sung, Jaemyoung, Negishi, Naoko, Nagino, Ken, Okumura, Yuichi, Miura, Maria, Shokirova, Hurramhon, Kuwahara, Mizu, Hirosawa, Kunihiko, Midorikawa-Inomata, Akie, Eguchi, Atsuko, Huang, Tianxiang, Yagita, Hideo, Habu, Sonoko, Okumura, Ko, and Murakami, Akira

Published
2022
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14. A high-sensitivity ELISA for detection of human FGF18 in culture supernatants from tumor cell lines

Author

Tsuchiya, Yuichi, primary, Komazawa-Sakon, Sachiko, additional, Tanaka, Masato, additional, Kanokogi, Takumi, additional, Moriwaki, Kenta, additional, Akiba, Hisaya, additional, Yagita, Hideo, additional, Okumura, Ko, additional, Entzminger, Kevin C., additional, Okumura, C.J., additional, Maruyama, Toshiaki, additional, and Nakano, Hiroyasu, additional

Published
2023
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15. Bortezomib Improves Adoptive T-cell Therapy by Sensitizing Cancer Cells to FasL Cytotoxicity

Author

Shanker, Anil, Pellom, Samuel T, Dudimah, Duafalia F, Thounaojam, Menaka C, de Kluyver, Rachel L, Brooks, Alan D, Yagita, Hideo, McVicar, Daniel W, Murphy, William J, Longo, Dan L, and Sayers, Thomas J

Subjects
Immunization, Rare Diseases, Vaccine Related, Cancer, 1.1 Normal biological development and functioning, 5.2 Cellular and gene therapies, Development of treatments and therapeutic interventions, Underpinning research, Animals, Antineoplastic Agents, Bortezomib, Combined Modality Therapy, Cytotoxicity, Immunologic, Fas Ligand Protein, Flow Cytometry, Humans, Immunoblotting, Immunohistochemistry, Immunotherapy, Adoptive, Kidney Neoplasms, Melanoma, Mice, Mice, Inbred BALB C, Mice, Knockout, T-Lymphocytes, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

Cancer immunotherapy shows great promise but many patients fail to show objective responses, including in cancers that can respond well, such as melanoma and renal adenocarcinoma. The proteasome inhibitor bortezomib sensitizes solid tumors to apoptosis in response to TNF-family death ligands. Because T cells provide multiple death ligands at the tumor site, we investigated the effects of bortezomib on T-cell responses in immunotherapy models involving low-avidity antigens. Bortezomib did not affect lymphocyte or tissue-resident CD11c(+)CD8(+) dendritic cell counts in tumor-bearing mice, did not inhibit dendritic cell expression of costimulatory molecules, and did not decrease MHC class I/II-associated antigen presentation to cognate T cells. Rather, bortezomib activated NF-κB p65 in CD8(+) T cells, stabilizing expression of T-cell receptor CD3ζ and IL2 receptor-α, while maintaining IFNγ secretion to improve FasL-mediated tumor lysis. Notably, bortezomib increased tumor cell surface expression of Fas in mice as well as human melanoma tissue from a responsive patient. In renal tumor-bearing immunodeficient Rag2(-/-) mice, bortezomib treatment after adoptive T-cell immunotherapy reduced lung metastases and enhanced host survival. Our findings highlight the potential of proteasome inhibitors to enhance antitumor T-cell function in the context of cancer immunotherapy.

Published
2015

18. CD39+PD-1+CD8+ T cells mediate metastatic dormancy in breast cancer

Author

Tallón de Lara, Paulino, Castañón, Héctor, Vermeer, Marijne, Núñez, Nicolás, Silina, Karina, Sobottka, Bettina, Urdinez, Joaquín, Cecconi, Virginia, Yagita, Hideo, Movahedian Attar, Farkhondeh, Hiltbrunner, Stefanie, Glarner, Isabelle, Moch, Holger, Tugues, Sònia, Becher, Burkhard, and van den Broek, Maries

Published
2021
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19. Interleukin-11-expressing fibroblasts have a unique gene signature correlated with poor prognosis of colorectal cancer

Author

Nishina, Takashi, Deguchi, Yutaka, Ohshima, Daisuke, Takeda, Wakami, Ohtsuka, Masato, Shichino, Shigeyuki, Ueha, Satoshi, Yamazaki, Soh, Kawauchi, Mika, Nakamura, Eri, Nishiyama, Chiharu, Kojima, Yuko, Adachi-Akahane, Satomi, Hasegawa, Mizuho, Nakayama, Mizuho, Oshima, Masanobu, Yagita, Hideo, Shibuya, Kazutoshi, Mikami, Tetuo, Inohara, Naohiro, Matsushima, Kouji, Tada, Norihiro, and Nakano, Hiroyasu

Published
2021
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20. Impaired Bone Resorption and Woven Bone Formation Are Associated with Development of Osteonecrosis of the Jaw-Like Lesions by Bisphosphonate and Anti–Receptor Activator of NF-κB Ligand Antibody in Mice

Author

Williams, Drake W, Lee, Cindy, Kim, Terresa, Yagita, Hideo, Wu, Hongkun, Park, Sil, Yang, Paul, Liu, Honghu, Shi, Songtao, Shin, Ki-Hyuk, Kang, Mo K, Park, No-Hee, and Kim, Reuben H

Subjects
Biomedical and Clinical Sciences, Dentistry, Dental/Oral and Craniofacial Disease, 2.1 Biological and endogenous factors, 1.1 Normal biological development and functioning, Underpinning research, Aetiology, Animals, Antibodies, Monoclonal, Humanized, Bisphosphonate-Associated Osteonecrosis of the Jaw, Bone Resorption, Denosumab, Diphosphonates, Disease Models, Animal, Imidazoles, Mice, Osteoclasts, RANK Ligand, Zoledronic Acid, Medical and Health Sciences, Pathology, Biomedical and clinical sciences, Health sciences
Abstract

Drug-induced osteonecrosis of the jaw (ONJ) is a detrimental intraoral lesion that often occurs after dental-related interventions in patients undergoing treatment with bisphosphonates or denosumab, the neutralizing human anti-receptor activator of NF-κB ligand (RANKL) antibody (Ab). The cause of ONJ by these drugs has been speculated to their direct effects on osteoclasts. However, the extent to which osteoclasts contribute to ONJ pathogenesis remains controversial. Herein, by using a tooth-extraction mouse model with i.v. administration of mouse anti-RANKL Ab or the bisphosphonate zoledronate (ZOL), we show that unresorbed bone due to impaired formation or suppressed functions of osteoclasts, respectively, is associated with ONJ development. After tooth extraction, ONJ-like lesions developed 50% in the anti-RANKL Ab-treated mice and 30% in the ZOL-treated mice. Nonviable and unresorbed bone was found more in anti-RANKL Ab-treated mice compared with mice receiving ZOL. All mice receiving anti-RANKL Ab had an undetectable tartrate-resistant acid phosphatase (TRAP) level in the serum and no TRAP-positive osteoclasts at the extracted sockets, whereas ZOL-treated mice had a decreased TRAP level without altering the numbers of TRAP-positive osteoclasts. Interestingly, the absence of newly formed woven bone in the extracted sockets was evident in ONJ-like lesions from both anti-RANKL Ab- and ZOL-treated mice. Our study suggests that the lack of osteoclasts' bone-resorptive functions by these drugs and suppression of woven bone formation after dental trauma may be associated with ONJ development.

Published
2014

21. Regulatory T Cells and Myeloid-Derived Suppressor Cells in the Tumor Microenvironment Undergo Fas-Dependent Cell Death during IL-2/αCD40 Therapy

Author

Weiss, Jonathan M, Subleski, Jeff J, Back, Tim, Chen, Xin, Watkins, Stephanie K, Yagita, Hideo, Sayers, Thomas J, Murphy, William J, and Wiltrout, Robert H

Subjects
Vaccine Related, Cancer, Clinical Research, Immunization, Development of treatments and therapeutic interventions, 5.2 Cellular and gene therapies, Animals, Antineoplastic Agents, CD40 Antigens, CD8-Positive T-Lymphocytes, Cell Death, Cell Line, Tumor, Interleukin-2, Mice, Mice, Inbred BALB C, Mice, Knockout, Myeloid Cells, Neoplasms, Experimental, Proto-Oncogene Proteins c-bcl-2, T-Lymphocytes, Regulatory, Tumor Microenvironment, fas Receptor, Immunology
Abstract

Fas ligand expression in certain tumors has been proposed to contribute to immunosuppression and poor prognosis. However, immunotherapeutic approaches may elicit the Fas-mediated elimination of immunosuppressive regulatory T cells (Tregs) and myeloid-derived suppressor cells (MDSCs) within tumors that represent major obstacles for cancer immunotherapy. Previously, we showed that IL-2 and agonistic CD40 Ab (αCD40) elicited synergistic antitumor responses coincident with the efficient removal of Tregs and MDSCs. We demonstrate in this study in two murine tumor models that Treg and MDSC loss within the tumor microenvironment after IL-2/αCD40 occurs through a Fas-dependent cell death pathway. Among tumor-infiltrating leukocytes, CD8(+) T cells, neutrophils, and immature myeloid cells expressed Fas ligand after treatment. Fas was expressed by tumor-associated Tregs and immature myeloid cells, including MDSCs. Tregs and MDSCs in the tumor microenvironment expressed active caspases after IL-2/αCD40 therapy and, in contrast with effector T cells, Tregs significantly downregulated Bcl-2 expression. In contrast, Tregs and MDSCs proliferated and expanded in the spleen after treatment. Adoptive transfer of Fas-deficient Tregs or MDSCs into wild-type, Treg-, or MDSC-depleted hosts resulted in the persistence of Tregs or MDSCs and the loss of antitumor efficacy in response to IL-2/αCD40. These results demonstrate the importance of Fas-mediated Treg/MDSC removal for successful antitumor immunotherapy. Our results suggest that immunotherapeutic strategies that include exploiting Treg and MDSC susceptibility to Fas-mediated apoptosis hold promise for treatment of cancer.

Published
2014

24. Antigen delivery targeted to tumor-associated macrophages overcomes tumor immune resistance

Author

Muraoka, Daisuke, Seo, Naohiro, Hayashi, Tae, Tahara, Yoshiro, Fujii, Keisuke, Tawara, Isao, Miyahara, Yoshihiro, Okamori, Kana, Yagita, Hideo, Imoto, Seiya, Yamaguchi, Rui, Komura, Mitsuhiro, Miyano, Satoru, Goto, Masahiro, Sawada, Shin-Ichi, Asai, Akira, Ikeda, Hiroaki, Akiyoshi, Kazunari, Harada, Naozumi, and Shiku, Hiroshi

Subjects
Antigens -- Health aspects, Cancer patients -- Health aspects, Cell death -- Research, Immunotherapy -- Usage, Macrophages -- Research, T cells, Peptides, Tumors, Trabectedin, Immune response, Genes, Inflammation, Health care industry
Abstract

Immune checkpoint inhibitors and adoptive transfer of gene-engineered T cells have emerged as novel therapeutic modalities for hard-to-treat solid tumors; however, many patients are refractory to these immunotherapies, and the mechanisms underlying tumor immune resistance have not been fully elucidated. By comparing the tumor microenvironment of checkpoint inhibition-sensitive and -resistant murine solid tumors, we observed that the resistant tumors had low immunogenicity. We identified antigen presentation by [CD11b.sup.+][F4/80.sup.+] tumor-associated macrophages (TAMs) as a key factor correlated with immune resistance. In the resistant tumors, TAMs remained inactive and did not exert antigen-presenting activity. Targeted delivery of a long peptide antigen to TAMs by using a nano- sized hydrogel (nanogel) in the presence of a TLR agonist activated TAMs, induced their antigen-presenting activity, and thereby transformed the resistant tumors into tumors sensitive to adaptive immune responses such as adoptive transfer of tumor-specific T cell receptor-engineered T cells. These results indicate that the status and function of TAMs have a significant impact on tumor immune sensitivity and that manipulation of TAM functions would be an effective approach for improving the efficacy of immunotherapies., Introduction Accumulating preclinical and clinical evidence has shown that inhibition of immune checkpoint proteins, such as cytotoxic lymphocyte- associated protein 4 (CTLA-4), programmed cell death receptor 1 (PD-1), and programmed [...]

Published
2019
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31. Data from Dietary Lactobacillus-Derived Exopolysaccharide Enhances Immune-Checkpoint Blockade Therapy

Author

Kawanabe-Matsuda, Hirotaka, primary, Takeda, Kazuyoshi, primary, Nakamura, Marie, primary, Makino, Seiya, primary, Karasaki, Takahiro, primary, Kakimi, Kazuhiro, primary, Nishimukai, Megumi, primary, Ohno, Tatsukuni, primary, Omi, Jumpei, primary, Kano, Kuniyuki, primary, Uwamizu, Akiharu, primary, Yagita, Hideo, primary, Boneca, Ivo Gomperts, primary, Eberl, Gérard, primary, Aoki, Junken, primary, Smyth, Mark J., primary, and Okumura, Ko, primary

Published
2023
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32. Supplementary Figure from Dietary Lactobacillus-Derived Exopolysaccharide Enhances Immune-Checkpoint Blockade Therapy

Author

Kawanabe-Matsuda, Hirotaka, primary, Takeda, Kazuyoshi, primary, Nakamura, Marie, primary, Makino, Seiya, primary, Karasaki, Takahiro, primary, Kakimi, Kazuhiro, primary, Nishimukai, Megumi, primary, Ohno, Tatsukuni, primary, Omi, Jumpei, primary, Kano, Kuniyuki, primary, Uwamizu, Akiharu, primary, Yagita, Hideo, primary, Boneca, Ivo Gomperts, primary, Eberl, Gérard, primary, Aoki, Junken, primary, Smyth, Mark J., primary, and Okumura, Ko, primary

Published
2023
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33. Supplementary Table from Dietary Lactobacillus-Derived Exopolysaccharide Enhances Immune-Checkpoint Blockade Therapy

Author

Kawanabe-Matsuda, Hirotaka, primary, Takeda, Kazuyoshi, primary, Nakamura, Marie, primary, Makino, Seiya, primary, Karasaki, Takahiro, primary, Kakimi, Kazuhiro, primary, Nishimukai, Megumi, primary, Ohno, Tatsukuni, primary, Omi, Jumpei, primary, Kano, Kuniyuki, primary, Uwamizu, Akiharu, primary, Yagita, Hideo, primary, Boneca, Ivo Gomperts, primary, Eberl, Gérard, primary, Aoki, Junken, primary, Smyth, Mark J., primary, and Okumura, Ko, primary

Published
2023
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41. Insulin-induced remission in new-onset NOD mice is maintained by the PD-1–PD-L1 pathway

Author

Fife, Brian T, Guleria, Indira, Bupp, Melanie Gubbels, Eagar, Todd N, Tang, Qizhi, Bour-Jordan, Helene, Yagita, Hideo, Azuma, Miyuki, Sayegh, Mohamed H, and Bluestone, Jeffrey A

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Immunology, Immunization, Diabetes, Vaccine Related, Aetiology, 2.1 Biological and endogenous factors, Metabolic and endocrine, Animals, Antigens, Surface, Apoptosis Regulatory Proteins, B7-1 Antigen, B7-H1 Antigen, Cells, Cultured, Diabetes Mellitus, Type 1, Female, Immune Tolerance, Insulin, Membrane Glycoproteins, Mice, Mice, Inbred NOD, Peptides, Programmed Cell Death 1 Receptor, Remission Induction, Signal Transduction, Medical and Health Sciences, Biomedical and clinical sciences, Health sciences
Abstract

The past decade has seen a significant increase in the number of potentially tolerogenic therapies for treatment of new-onset diabetes. However, most treatments are antigen nonspecific, and the mechanism for the maintenance of long-term tolerance remains unclear. In this study, we developed an antigen-specific therapy, insulin-coupled antigen-presenting cells, to treat diabetes in nonobese diabetic mice after disease onset. Using this approach, we demonstrate disease remission, inhibition of pathogenic T cell proliferation, decreased cytokine production, and induction of anergy. Moreover, we show that robust long-term tolerance depends on the programmed death 1 (PD-1)-programmed death ligand (PD-L)1 pathway, not the distinct cytotoxic T lymphocyte-associated antigen 4 pathway. Anti-PD-1 and anti-PD-L1, but not anti-PD-L2, reversed tolerance weeks after tolerogenic therapy by promoting antigen-specific T cell proliferation and inflammatory cytokine production directly in infiltrated tissues. PD-1-PD-L1 blockade did not limit T regulatory cell activity, suggesting direct effects on pathogenic T cells. Finally, we describe a critical role for PD-1-PD-L1 in another powerful immunotherapy model using anti-CD3, suggesting that PD-1-PD-L1 interactions form part of a common pathway to selectively maintain tolerance within the target tissues.

Published
2006

48. Supplementary Tables 1 through 3 from Systemic DC Activation Modulates the Tumor Microenvironment and Shapes the Long-Lived Tumor-Specific Memory Mediated by CD8+ T Cells

Author

Shimizu, Kanako, primary, Yamasaki, Satoru, primary, Shinga, Jun, primary, Sato, Yusuke, primary, Watanabe, Takashi, primary, Ohara, Osamu, primary, Kuzushima, Kiyotaka, primary, Yagita, Hideo, primary, Komuro, Yoshiko, primary, Asakura, Miki, primary, and Fujii, Shin-ichiro, primary

Published
2023
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