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Your search keyword '"Motoi, Natsuki"' showing total 19 results
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19 results on '"Motoi, Natsuki"'

1. Direct evidence that GM-CSF inhalation improves lung clearance in pulmonary alveolar proteinosis

Author

Ohashi, Kazumasa, Sato, Atsuyasu, Takada, Toshinori, Arai, Toru, Nei, Takahito, Kasahara, Yasunori, Motoi, Natsuki, Hojo, Masayuki, Urano, Shinya, Ishii, Haruyuki, Yokoba, Masanori, Eda, Ryosuke, Nakayama, Hideaki, Nasuhara, Yasuyuki, Tsuchihashi, Yoshiko, Kaneko, Chinatsu, Kanazawa, Hiroko, Ebina, Masahito, Yamaguchi, Etsuro, Kirchner, Jacqueline, Inoue, Yoshikazu, Nakata, Koh, and Tazawa, Ryushi

Published
2012
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6. Memory B cell pool of autoimmune pulmonary alveolar proteinosis patients contains higher frequency of GM-CSF autoreactive B cells than healthy subjects

Author

Nei, Takahito, primary, Urano, Shinya, additional, Motoi, Natsuki, additional, Hashimoto, Atsushi, additional, Kitamura, Nobutaka, additional, Tanaka, Takahiro, additional, Nakagaki, Kazuhide, additional, Takizawa, Jun, additional, Kaneko, Chinatsu, additional, Tazawa, Ryushi, additional, and Nakata, Koh, additional

Published
2019
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7. Light chain (κ/λ) ratio of GM-CSF autoantibodies is associated with disease severity in autoimmune pulmonary alveolar proteinosis

Author

Nei, Takahito, primary, Urano, Shinya, additional, Itoh, Yuko, additional, Kitamura, Nobutaka, additional, Hashimoto, Atsushi, additional, Tanaka, Takahiro, additional, Motoi, Natsuki, additional, Kaneko, Chinatsu, additional, Tazawa, Ryushi, additional, Nakagaki, Kazuhide, additional, Arai, Toru, additional, Inoue, Yoshikazu, additional, and Nakata, Koh, additional

Published
2013
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8. IgM-type GM-CSF autoantibody is etiologically a bystander but associated with IgG-type autoantibody production in autoimmune pulmonary alveolar proteinosis

Author

Nei, Takahito, primary, Urano, Shinya, additional, Motoi, Natsuki, additional, Takizawa, Jun, additional, Kaneko, Chinatsu, additional, Kanazawa, Hiroko, additional, Tazawa, Ryushi, additional, Nakagaki, Kazuhide, additional, Akagawa, Kiyoko S., additional, Akasaka, Keiichi, additional, Ichiwata, Toshio, additional, Azuma, Arata, additional, and Nakata, Koh, additional

Published
2012
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19. IgM-type GM-CSF autoantibody is etiologically a bystander but associated with IgG-type autoantibody production in autoimmune pulmonary alveolar proteinosis.

Author

Nei T, Urano S, Motoi N, Takizawa J, Kaneko C, Kanazawa H, Tazawa R, Nakagaki K, Akagawa KS, Akasaka K, Ichiwata T, Azuma A, and Nakata K

Subjects
Adolescent, Adult, Aged, Antibody Formation, Autoantibodies chemistry, Autoantibodies physiology, Bronchoalveolar Lavage Fluid chemistry, Case-Control Studies, Cell Count, Child, Female, Granulocyte-Macrophage Colony-Stimulating Factor chemistry, Humans, Immunoglobulin A blood, Immunoglobulin G blood, Immunoglobulin G chemistry, Immunoglobulin M chemistry, Immunoglobulin M physiology, Leukocytes, Mononuclear cytology, Leukocytes, Mononuclear metabolism, Male, Middle Aged, Protein Binding, Young Adult, Autoantibodies blood, Autoimmune Diseases immunology, Granulocyte-Macrophage Colony-Stimulating Factor immunology, Immunoglobulin G biosynthesis, Immunoglobulin M blood, Pulmonary Alveolar Proteinosis immunology
Abstract

The granulocyte-macrophage colony-stimulating factor (GM-CSF) autoantibody (GMAb) is the causative agent underlying autoimmune pulmonary alveolar proteinosis (aPAP). It consists primarily of the IgG isotype. At present, information on other isotypes of the autoantibody is limited. We detected serum the IgM isotype of GMAb (IgM-GMAb) in more than 80% of patients with aPAP and 22% of healthy subjects, suggesting that a continuous antigen pressure may be present in most patients. Levels of the IgM isotype were weakly correlated with IgG-GMAb levels but not IgA-GMAb, suggesting that its production may be associated with that of IgG-GMAb. The mean binding avidity to GM-CSF of the IgM isotype was 100-fold lower than the IgG-GMAb isotype, whereas the IC(50) value for neutralizing capacity was 20,000-fold higher than that of IgG-GMAb, indicating that IgM-GMAb is only a very weak neutralizer of GM-CSF. In bronchoalveolar lavage fluid from nine patients, IgG-GMAb was consistently detected, but IgM-GMAb was under the detection limit in most patients, confirming that IgM-GMAb is functionally a bystander in the pathogenesis of aPAP. It rather may be involved in the mechanism for development of IgG-GMAb in vivo.

Published
2012
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