CD28 co-stimulatory signals induced IL-2 receptor expression on antigen-stimulated virgin T cells by an IL-2- independent mechanism.
スポンサーリンク
概要
著者
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Yohko Takahashi
Institute Of Immunological Science Hokkaido University
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Ryo Abe
Research Institute For Biological Science Science University Of Tokyo Department Of Dermatology Asah
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Xu-guang Tai
Biomedical Research Center Osaka Universitiy Medical School
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Kazuhito Toyooka
Biomedical Research Center, Osaka Universitiy Medical School
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Seiji Maruo
Biomedical Research Center, Osaka Universitiy Medical School
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Tohru Iwahori
Biomedical Research Center, Osaka Universitiy Medical School
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Norihiko Yamamoto
Biomedical Research Center, Osaka Universitiy Medical School
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Ryo Abe
Immune Cell Biology Program, Naval Medical Research Institute
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Yousuke Takahama
Syntex Institute of Immunology
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Masaaki Murakami
Institute of Immunological Science, Hokkaido University
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Toshimitsu Uede
Institute of Immunological Science, Hokkaido University
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Toshiyuki Hamaoka
Biomedical Research Center, Osaka Universitiy Medical School
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Hiromi FujiWara
Biomedical Research Center, Osaka Universitiy Medical School
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Tohru Iwahori
Biomedical Research Center Osaka Universitiy Medical School
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Seiji Maruo
Biomedical Research Center Osaka Universitiy Medical School
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Hiromi Fujiwara
Biomedical Research Center Osaka Universitiy Medical School
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Masaaki Murakami
Section Of Immunopathogenesis Institute Of Immunological Science Hokkaido University
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Kazuhito Toyooka
Biomedical Research Center Osaka Universitiy Medical School
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Toshiyuki Hamaoka
Biomedical Research Center Osaka Universitiy Medical School
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Toshimitsu Uede
Institute Of Immunologiacal Science Hokkaido University
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Masaaki Murakami
Institute Of Immunlogical Science Hokkaido University
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Norihiko Yamamoto
Biomedical Research Center Osaka Universitiy Medical School
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Toshimitsu Uede
Division Of Developmental Genetics Center For Biomedical Science Chiba University School Of Medicine
関連論文
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- CD28 co-stimulatory signals induced IL-2 receptor expression on antigen-stimulated virgin T cells by an IL-2- independent mechanism.
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