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260 results on '"Kashiwakura, Jun-ichi"'

4. Role of Signal-Transducing Adaptor Protein-1 for T Cell Activation and Pathogenesis of Autoimmune Demyelination and Airway Inflammation

Author

Kagohashi, Kota, primary, Sasaki, Yuto, additional, Ozawa, Kiyotaka, additional, Tsuchiya, Takuya, additional, Kawahara, Shoya, additional, Saitoh, Kodai, additional, Ichii, Michiko, additional, Toda, Jun, additional, Harada, Yasuyo, additional, Kubo, Masato, additional, Kitai, Yuichi, additional, Muromoto, Ryuta, additional, Oritani, Kenji, additional, Kashiwakura, Jun-ichi, additional, and Matsuda, Tadashi, additional

Published
2024
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8. Differentiation between control subjects and patients with chronic spontaneous urticaria based on the ability of anti-IgE autoantibodies (AAbs) to induce FcεRI crosslinking, as compared to anti-FcεRIα AAbs

Author

Izaki, Satoshi, Toyoshima, Shota, Endo, Takahiro, Kanegae, Kazuko, Nunomura, Satoshi, Kashiwakura, Jun-ichi, Sasaki-Sakamoto, Tomomi, Nakamura, Ryosuke, Akiyama, Haruyo, Ra, Chisei, Hayama, Koremasa, Terui, Tadashi, and Okayama, Yoshimichi

Published
2019
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9. STAP‐2 negatively regulates BCR‐mediated B cell activation by recruiting tyrosine‐protein kinase CSK to LYN

Author

Kashiwakura, Jun‐ichi, primary, Kawahara, Shoya, additional, Inagaki, Iori, additional, Inui, Kyosuke, additional, Saitoh, Kodai, additional, Kagohashi, Kota, additional, Sasaki, Yuto, additional, Kobayashi, Fuki, additional, Kitai, Yuichi, additional, Muromoto, Ryuta, additional, Oritani, Kenji, additional, and Matsuda, Tadashi, additional

Published
2023
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13. Histamine-releasing factor enhances food allergy

Author

Ando, Tomoaki, Kashiwakura, Jun-ichi, Itoh-Nagato, Naoka, Yamashita, Hirotaka, Baba, Minato, Kawakami, Yu, Tsai, Shih Han, Inagaki, Naoki, Takeda, Kiyoshi, Iwata, Tsutomu, Shimojo, Naoki, Fujisawa, Takao, Nagao, Mizuho, Matsumoto, Kenji, Kawakami, Yuko, and Kawakami, Toshiaki

Subjects
B cells -- Health aspects, Cytokines -- Analysis, Inflammation -- Risk factors, Food hypersensitivity -- Health aspects, Immunoglobulin E -- Health aspects, Health care industry
Abstract

Food allergy occurs due to IgE- and mast cell-dependent Intestinal Inflammation. Previously, we showed that histaminereleasing factor (HRF), a multifunctional protein secreted during allergy, interacts with a subset of IgE molecules and that the HRF dimer activates mast cells in an HRF-reactive IgE-dependent manner. In this study, we investigated whether HRF plays any role in food allergy. Specifically, we determined that prophylactic and therapeutic administration of HRF inhibitors that block HRF-IgE interactions reduces the incidence of diarrhea and mastocytosis in a murine model of food allergy. Food allergy-associated intestinal inflammation was accompanied by increased secretion of the HRF dimer into the intestine in response to proinflammatory, Th2, and epithelial-derived cytokines and HRF-reactive IgE levels at the elicitation phase. Consistent with these data, patients with egg allergy had higher blood levels of HRF-reactive IgE compared with individuals that were not hypersensitive. Successful oral immunotherapy in egg-allergy patients and food-allergic mice reduced HRF-reactive IgE levels, thereby suggesting a pathological role for HRF in food allergy. Together, these results suggest that antigen and HRF dimer amplify intestinal inflammation by synergistically activating mast cells and indicate that HRF has potential as a therapeutic target in food allergy., Introduction The prevalence of food allergy has been dramatically increasing for the last few decades (1, 2). Six to eight percent of children under the age of 3 have food [...]

Published
2017
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16. Mast cells play role in wound healing through the ZnT2/GPR39/IL-6 axis

Author

Nishida, Keigo, Hasegawa, Aiko, Yamasaki, Satoru, Uchida, Ryota, Ohashi, Wakana, Kurashima, Yosuke, Kunisawa, Jun, Kimura, Shunsuke, Iwanaga, Toshihiko, Watarai, Hiroshi, Hase, Koji, Ogura, Hideki, Nakayama, Manabu, Kashiwakura, Jun-ichi, Okayama, Yoshimichi, Kubo, Masato, Ohara, Osamu, Kiyono, Hiroshi, Koseki, Haruhiko, Murakami, Masaaki, and Hirano, Toshio

Published
2019
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20. Identification of RPL15 60S Ribosomal Protein as a Novel Topotecan Target Protein That Correlates with DAMP Secretion and Antitumor Immune Activation

Author

Yamada, Shunsuke, primary, Kitai, Yuichi, additional, Tadokoro, Takashi, additional, Takahashi, Runa, additional, Shoji, Haruka, additional, Maemoto, Taiga, additional, Ishiura, Marie, additional, Muromoto, Ryuta, additional, Kashiwakura, Jun-ichi, additional, Ishii, Ken J., additional, Maenaka, Katsumi, additional, Kawai, Taro, additional, and Matsuda, Tadashi, additional

Published
2022
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22. STAP-2 Is a Novel Positive Regulator of TCR-Proximal Signals

Author

Saitoh, Kodai, primary, Kashiwakura, Jun-ichi, additional, Kagohashi, Kota, additional, Sasaki, Yuto, additional, Kawahara, Shoya, additional, Sekine, Yuichi, additional, Kitai, Yuichi, additional, Muromoto, Ryuta, additional, Ichii, Michiko, additional, Nakatsukasa, Hiroko, additional, Yoshimura, Akihiko, additional, Oritani, Kenji, additional, and Matsuda, Tadashi, additional

Published
2022
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31. Signal-transducing adaptor protein-2 has a nonredundant role for IL-33-triggered mast cell activation

Author

Kashiwakura, Jun-ichi, primary, Koizumi, Nao, additional, Saitoh, Kodai, additional, Kagohashi, Kota, additional, Sasaki, Yuto, additional, Kobayashi, Fuki, additional, Kawahara, Shoya, additional, Yamauchi, Yukie, additional, Kitai, Yuichi, additional, Muromoto, Ryuta, additional, Oritani, Kenji, additional, and Matsuda, Tadashi, additional

Published
2021
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32. STAP-2 positively regulates Fc epsilon RI-mediated basophil activation and basophil-dependent allergic inflammatory reactions

Author

Kashiwakura, Jun-ichi, Yamashita, Shinsuke, Yoshihara, Mari, Inui, Kyosuke, Saitoh, Kodai, Sekine, Yuichi, Muromoto, Ryuta, Kitai, Yuichi, Oritani, Kenji, and Matsuda, Tadashi

Subjects
IgE-CAI, IL-4, STAP-2, IgE, basophils
Abstract

Basophils are an important cell type in the regulation of T(h)2 immune responses. Recently, we revealed that signal-transducing adaptor protein-2 (STAP-2) negatively regulates mast cell activation via Fc epsilon RI. However, the role of STAP-2 in basophil maturation and activation remained unclear. In this study, we demonstrated the normal development of basophils in STAP-2-deficient (STAP-2(-/-)) mice. We also demonstrated in vitro normal basophil differentiation and FceRI expression in STAP2(-/-) mice, suggesting that STAP-2 is dispensable for basophil maturation. Using bone marrow-derived cultured basophils (BMBs), we showed that degranulation and cytokine production of STAP-2(-/-) BMBs were lower than those of wild-type (WT) BMBs upon stimulation with IgE/Ag. In accordance with the reduction of degranulation and cytokine production, phosphorylation of several signal molecules such as Lyn, PLC-gamma 2 and Erk was reduced in STAP-2(-/-) BMBs after stimulation via Fc epsilon RI. Finally, it was observed that IgE-dependent chronic allergic inflammation of STAP-2(-/-) mice was significantly inhibited compared with WT mice. Taken together, we conclude that STAP-2 is an adaptor molecule that positively regulates FceRI-mediated basophil activation and basophil-dependent allergic inflammatory reactions.

Published
2019

35. Correction: Expression of signal-transducing adaptor protein-1 attenuates experimental autoimmune hepatitis via down-regulating activation and homeostasis of invariant natural killer T cells

Author

Kashiwakura, Jun-ichi, primary, Saitoh, Kodai, additional, Ihara, Takeru, additional, Sasaki, Yuto, additional, Kagohashi, Kota, additional, Enohara, Shiyo, additional, Morioka, Yuka, additional, Watarai, Hiroshi, additional, Muromoto, Ryuta, additional, Kitai, Yuichi, additional, Iwabuchi, Kazuya, additional, Oritani, Kenji, additional, and Matsuda, Tadashi, additional

Published
2021
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36. Histamine-releasing factor has a proinflammatory role in mouse models of asthma and allergy

Author

Kashiwakura, Jun-ichi, Ando, Tomoaki, Matsumoto, Kenji, Kimura, Miho, Kitaura, Jiro, Matho, Michael H., Zajonc, Dirk M., Ozeki, Tomomitsu, Ra, Chisei, MacDonald, Susan M., Siraganian, Reuben P., Broide, David H., Kawakami, Yuko, and Kawakami, Toshiaki

Subjects
Inflammation -- Diagnosis -- Care and treatment -- Research, Histamine -- Health aspects -- Research, Immunoglobulin E -- Physiological aspects -- Research, Asthma -- Analysis -- Diagnosis -- Care and treatment -- Research, Health care industry
Abstract

IgE-mediated activation of mast cells and basophils underlies allergic diseases such as asthma. Histamine-releasing factor (HRF; also known as translationally controlled tumor protein [TCTP] and fortilin) has been implicated in late-phase allergic reactions (LPRs) and chronic allergic inflammation, but its functions during asthma are not well understood. Here, we identified a subset of IgE and IgG antibodies as HRF-interacting molecules in vitro. HRF was able to dimerize and bind to Igs via interactions of its N-terminal and internal regions with the Fab region of Igs. Therefore, HRF together with HRF-reactive IgE was able to activate mast cells in vitro. In mouse models of asthma and allergy, Ig-interacting HRF peptides that were shown to block HRF/Ig interactions in vitro inhibited IgE/HRF-induced mast cell activation and in vivo cutaneous anaphylaxis and airway inflammation. Intranasally administered HRF recruited inflammatory immune cells to the lung in naive mice in a mast cell-and Fc receptor-dependent manner. These results indicate that HRF has a proinflammatory role in asthma and skin immediate hypersensitivity, leading us to suggest HRF as a potential therapeutic target., Introduction Mast cells and basophils are key effector cells for IgE-dependent allergic inflammatory reactions (1). Upon activation, these cells secrete preformed proinflammatory chemical mediators (e.g., histamine, proteases, proteoglycans, and nucleotides) [...]

Published
2012
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37. novel intramolecular negative regulation of mouse Jak3 activity by tyrosine 820.

Author

Sekine, Yuichi, Kikkawa, Kazuna, Witthuhn, Bruce A, Kashiwakura, Jun-ichi, Muromoto, Ryuta, Kitai, Yuichi, Fujimuro, Masahiro, Oritani, Kenji, and Matsuda, Tadashi

Subjects
KINASES, TYROSINE, CYTOKINE receptors, MICE, STAT proteins, CELL growth
Abstract

Jak3, a member of the Janus kinase family, is essential for the cytokine receptor common gamma chain (γc)-mediated signaling. During activation of Jak3, tyrosine residues are phosphorylated and potentially regulate its kinase activity. We identified a novel tyrosine phosphorylation site within mouse Jak3, Y820, which is conserved in human Jak3, Y824. IL-2-induced tyrosine phosphorylation of Jak3 Y824 in human T cell line HuT78 cells was detected by using a phosphospecific, pY824, antibody. Mutation of mouse Jak3 Y820 to alanine (Y820A) showed increased autophosphorylation of Jak3 and enhanced signal transducer and activator of transcription 5 (STAT5) tyrosine phosphorylation and transcriptional activation. Stably expressed Jak3 Y820A in F7 cells, an IL-2 responsive mouse pro-B cell line Ba/F3, exhibited enhanced IL-2-dependent cell growth. Mechanistic studies demonstrated that interaction between Jak3 and STAT5 increased in Jak3 Y820A compared to wild-type Jak3. These data suggest that Jak3 Y820 plays a role in negative regulation of Jak3-mediated STAT5 signaling cascade upon IL-2-stimulation. We speculate that this occurs through an interaction promoted by the tyrosine phosphorylated Y820 or a conformational change by Y820 mutation with either the STAT directly or with the recruitment of molecules such as phosphatases via a SH2 interaction. Additional studies will focus on these interactions as Jak3 plays a crucial role in disease and health. [ABSTRACT FROM AUTHOR]

Published
2022
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39. Graft-versus-host disease develops in mice transplanted with lymphocyte-depleted bone marrow cells from signal-transducing adaptor protein-2 transgenic mice

Author

Saito, Hideaki, primary, Ichii, Michiko, additional, Toda, Jun, additional, Kitai, Yuichi, additional, Muromoto, Ryuta, additional, Kashiwakura, Jun-ichi, additional, Saitoh, Kodai, additional, Tanimura, Akira, additional, Yokota, Takafumi, additional, Shibayama, Hirohiko, additional, Matsuda, Tadashi, additional, Oritani, Kenji, additional, Kanakura, Yuzuru, additional, and Hosen, Naoki, additional

Published
2021
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42. Expression of signal-transducing adaptor protein-1 attenuates experimental autoimmune hepatitis via down-regulating activation and homeostasis of invariant natural killer T cells

Author

Kashiwakura, Jun-ichi, primary, Saitoh, Kodai, additional, Ihara, Takeru, additional, Sasaki, Yuto, additional, Kagohashi, Kota, additional, Enohara, Shiyo, additional, Morioka, Yuka, additional, Watarai, Hiroshi, additional, Muromoto, Ryuta, additional, Kitai, Yuichi, additional, Iwabuchi, Kazuya, additional, Oritani, Kenji, additional, and Matsuda, Tadashi, additional

Published
2020
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50. Biochanin A enhances ROR gamma activity through STAT3-mediated recruitment of NCOA1

Author

Takahashi, Miki, Muromoto, Ryuta, Kojima, Hiroyuki, Takeuchi, Shinji, Kitai, Yuichi, Kashiwakura, Jun-ichi, and Matsuda, Tadashi

Subjects
STAT3, IL-17, ROR gamma, Isoflavones
Abstract

Interleukin (IL)-17-producing T cells play important roles in autoimmunity, chronic inflammation and host protection against extracellular bacteria and fungi. The retinoic acid receptor-related orphan receptors (ROR) alpha and beta are key regulators of the IL-17-producing phenotype. We previously showed that the isoflavone biochanin A enhanced ROR-mediated transcriptional activity. Here, we investigated the possible mechanisms underlying this ROR activation. Biochanin A-treated murine thymoma EL4 and primary splenocytes demonstrated enhanced induction of IL-17. Biochanin A also induced tyrosine-phosphorylation of signal transducer and activator of transcription 3 (STAT3) in these cells. Stable knockdown of either ROR gamma or STAT3 in EL4 cells canceled biochanin A-induced upregulation of IL-17 expression. Importantly, biochanin A enhanced complex formation between ROR gamma and STAT3 or nuclear-receptor coactivator 1 (NCOA1). Furthermore, the biochanin A-induced ROR gamma-NCOA1 complex was disrupted by a dominant negative mutant of STAT3 or by the STAT3 specific inhibitor Stattic. These results suggest that biochanin A activates ROR gamma-dependent IL-17 transcription through the enhancement of STAT3 phosphorylation and STAT3-mediated recruitment of NCOA1 to ROR gamma. (C) 2017 Elsevier Inc. All rights reserved.

Published
2017

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