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15. Sperm whale myoglobin swMb

Author

Isogai, Y., primary, Imamura, H., additional, Nakae, S., additional, Sumi, T., additional, Takahashi, K., additional, Nakagawa, T., additional, Tsuneshige, A., additional, and Shirai, T., additional

Published
2018
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20. Role of regulatory and proinflammatory T-cell populations in allergic diseases

Author

Orihara, Kanami, Nakae, S., Pawankar, R., and Saito, H.

Subjects
Pulmonary and Respiratory Medicine, lcsh:Immunologic diseases. Allergy, Thymic stromal lymphopoietin, T cell, Immunology, mast cells, Review Article, Immunoglobulin E, regulatory T cells, Interleukin 21, Immune system, thymic stromal lymphopoietin, Immunology and Allergy, Medicine, helper T cells, biology, business.industry, medicine.anatomical_structure, Interleukin 13, Interleukin 12, biology.protein, Interleukin 17, interleukin 17, business, lcsh:RC581-607
Abstract

Regulatory T (Treg) cells are considered to inhibit the development of both type 1 (Th1) and type 2 helper T (Th2) cells. However, it is recently reported that there are reduced numbers of Treg cells in patients with allergic diseases as compared with individuals who have high levels of serum immunoglobulin E and blood eosinophils but are asymptomatic. Therefore, Treg cells may suppress the onset of allergic disease by down-regulating other types of immune cells besides Th1 and Th2 cells. The newly discovered interleukin 17-producing helper T cells that are responsible for autoimmune inflammatory diseases may counteract Treg cells even in allergic diseases. The Th2 cells that are capable of producing of high levels of tumor necrosis factor-α may also be involved in inflammation in allergic diseases. In this review, we further discuss the role of Th1, Th2, interleukin 17-producing helper T cells, and Treg cells in allergic diseases by using the balancing square model and the factors differentiating between patients with clinical manifestations of allergic symptomatic and atopic individuals who are sensitized but asymptomatic. Keywords: helper T cells, regulatory T cells, interleukin 17, mast cells, thymic stromal lymphopoietin

Published
2008

22. IL-33 signaling contributes to the pathogenesis of myeloproliferative neoplasms

Author

Mager, L F, Riether, C, Schürch, C M, Banz, Y, Wasmer, M H, Stuber, R, Theocharides, A P, Li, X, Xia, Y, Saito, H, Nakae, S, Baerlocher, G M, Manz, M G, McCoy, K D, Macpherson, A J, Ochsenbein, A F, Beutler, B, Krebs, P, University of Zurich, and Krebs, P

Subjects
10032 Clinic for Oncology and Hematology, 610 Medicine & health, 2700 General Medicine
Published
2015

23. STAT6 and IL‐10 are required for the anti‐arthritic effects of Schistosoma mansoni via different mechanisms.

Author

Osada, Y., Horie, Y., Nakae, S., Sudo, K., and Kanazawa, T.

Subjects
SCHISTOSOMA mansoni, ARTHRITIS, COLLAGEN, THICKNESS measurement
Abstract

Summary: To investigate possible roles of T helper type 2 (Th2) cytokines in the anti‐arthritic effects of a blood fluke, Schistosoma mansoni (Sm), for mouse collagen‐induced arthritis (CIA), wild‐type (WT), signal transducer and activator of transcription 6 (STAT6) knock‐out (KO) and interleukin (IL)‐10 KO mice were infected with Sm. Three weeks after infection, the mice were immunized with bovine type II collagen (IIC). Arthritis severity was monitored by scoring, measurement of paw thickness and the presence of ankylosis. Serum anti‐IIC IgG levels, splenic cytokine production and cytokine gene expression in the popliteal lymph nodes (PLNs) were measured and compared among WT and gene‐KO mice. Consistent with our previous findings, Sm infection reduced the arthritis severity in WT mice. Splenic production of IL‐17A and tumor necrosis factor (TNF)‐α was reduced by the infection. In contrast, Sm infection markedly exacerbated CIA in STAT6 KO mice. In the KO mice, IL‐17A production was increased by the infection. Conversely, Sm infection did not affect the exacerbated arthritis in IL‐10 KO mice, although IL‐17A production was reduced by the helminth. Our results suggest that signaling via STAT6 (presumably IL‐4 and/or IL‐13) and IL‐10 is required for the suppression of CIA by Sm infection, but through different mechanisms. STAT6 was essential for helminth‐induced reduction of IL‐17A, whereas regulation of the basal arthritis severity by IL‐10 was needed in order for it to be sufficiently suppressed by the helminth. Schistosoma mansoni infection reduces severity of collagen‐induced arthritis in mice. STAT6‐ mediated signaling and IL‐10 are essential for the anti‐arthritic effects of the helminth. [ABSTRACT FROM AUTHOR]

Published
2019
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25. Structure of EndoMS-dsDNA2 complex

Author

Nakae, S., primary, Hijikata, A., additional, Tsuji, T., additional, Yonezawa, K., additional, Kouyama, K., additional, Mayanagi, K., additional, Ishino, S., additional, Ishino, Y., additional, and Shirai, T., additional

Published
2016
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26. Structure of EndoMS in apo form

Author

Nakae, S., primary, Hijikata, A., additional, Tsuji, T., additional, Yonezawa, K., additional, Kouyama, K., additional, Mayanagi, K., additional, Ishino, S., additional, Ishino, Y., additional, and Shirai, T., additional

Published
2016
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33. IL-33 Receptor-Expressing Regulatory T Cells Are Highly Activated, Th2 Biased and Suppress CD4 T Cell Proliferation through IL-10 and TGFß Release

Author

Siede J Fröhlich A Datsi A Hegazy AN Varga DV Holecska V Saito H Nakae S Löhning M.

Subjects
hemic and immune systems, chemical and pharmacologic phenomena
Abstract

Immunomodulatory Foxp3+ regulatory T cells (Tregs) form a heterogeneous population consisting of subsets with different activation states migratory properties and suppressive functions. Recently expression of the IL 33 receptor ST2 was shown on Tregs in inflammatory settings. Here we report that ST2 expression identifies highly activated Tregs in mice even under homeostatic conditions. ST2+ Tregs preferentially accumulate at non lymphoid sites likely mediated by their high expression of several chemokine receptors facilitating tissue homing. ST2+ Tregs exhibit a Th2 biased character expressing GATA 3 and producing the Th2 cytokines IL 5 and IL 13 –especially in response to IL 33. Yet IL 33 is dispensable for the generation and maintenance of these cells in vivo. Furthermore ST2+ Tregs are superior to ST2- Tregs in suppressing CD4+ T cell proliferation in vitro independent of IL 33. This higher suppressive capacity is partially mediated by enhanced production and activation of the anti inflammatory cytokines IL 10 and TGFß. Thus ST2 expression identifies a highly activated strongly suppressive Treg subset preferentially located in non lymphoid tissues. Here ST2+ Tregs may be well positioned to immediately react to IL 33 alarm signals. Their specific properties may render ST2+ Tregs useful targets for immunomodulatory therapies.

Published
2016

35. TH2 cytokines potently induce an appetite-stimulating peptide, melanin-concentrating hormone, in human vascular endothelial cells

Author

Orihara, Kanami, Morita, H., Yagami, A., Kajiwara, N., Nakae, S., Matsumoto, K., Nagasaki, H., Saito, Y., Saito, H., and Matsuda, A.

Subjects
Melanin-concentrating hormone, Tumor Necrosis Factor-alpha/immunology/pharmacology, Appetite, Stimulation, Peptide, RNA, Small Interfering/metabolism, chemistry.chemical_compound, Mice, Immunology and Allergy, RNA, Small Interfering, Asthma/etiology/*genetics, chemistry.chemical_classification, Hypothalamic Hormones, Interleukin, Th2 Cells/drug effects/*immunology, Vascular endothelial growth factor B, Appetite/*genetics/immunology, medicine.anatomical_structure, Cytokines, Obesity/*complications, medicine.medical_specialty, Endothelium, Melanins/*genetics, Immunology, Interleukin-4/immunology/pharmacology, Biology, Th2 Cells, Internal medicine, medicine, Gene silencing, Animals, Humans, Obesity, Gene Silencing, STAT6 Transcription Factor/genetics/metabolism, Melanins, Chromosomes, Human, Pair 12/genetics, Chromosomes, Human, Pair 12, Tumor Necrosis Factor-alpha, Gene Expression Profiling, Endothelium, Vascular/drug effects/*immunology, Hypothalamic Hormones/*genetics, Asthma, Pituitary Hormones, Endocrinology, chemistry, Cytokines/*immunology/pharmacology, Endothelium, Vascular, Interleukin-4, STAT6 Transcription Factor, Pituitary Hormones/*genetics, Hormone
Published
2009

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