Zhang Xingmin | Center For Neurologic Diseases Harvard Medical School
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概要
関連著者
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ZHANG Xingmin
Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School
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Zhang Xingmin
Center For Neurologic Diseases Harvard Medical School
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Weiner H
Harvard Medical School Ma Usa
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Weiner Howard
Center For Neurologic Diseases Brigham And Women's Hospital Harvard Medical School
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Weiner Howard
Center For Neurologic Disease Brigham And Women's Hospital Harvard Medical School
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Kuchroo V
Center For Neurologic Diseases Brigham And Women's Hospital Harvard Medical School
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Kuchroo Vijay
Center For Neurologic Diseases Brigham And Women's Hospital Harvard Medical School
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Zhang Xianghua
Department Of Immunology National Jewish Medical And Research Center And University Of Colorado Scho
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Reddy Jayagopala
Center For Neurologic Diseases Brigham And Women's Hospital Harvard Medical School
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Li Li
Department of Gynecology, The People's Hospital of Xinjiang Province, Xinjiang Medical University
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Sherr David
Department Of Environmental Health School Of Public Health Boston University School Of Medicine
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Frenkel Dan
Center For Neurologic Diseases Brigham And Women's Hospital Harvard Medical School
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JU Shyr-te
Departments of Medicine and Pahology,and Laboratory Medicine, Boston University School of Medicine
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JODO Satoshi
Department of Medicine II, Hokkaido University Graduate School of Medicine
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SAKAGUCHI Shimon
Department of Experimental Pathology, Institute for Frontier Medical Sciences, Kyoto University
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Sakaguchi Shimon
Department Of Experimental Pathology Institute For Frontier Medical Sciences
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Ju S‐t
Department Of Pathology And Laboratory Medicine Boston University School Of Medicine
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Ju Shyr-te
Department Of Microbiology Center For Immunity Inflammation And Regenerative Medicine University Of
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Jodo Satoshi
Department Of Medicine Boston University School Of Medicine
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Ochi Hirofumi
Center For Neurologic Diseases Brigham And Women's Hospital Harvard Medical School
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Sakaguchi S
Department Of Immunopathology Tokyo Metropolitan Institute Of Gerontology
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KOLDZIC Djordje
Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School
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IZIKSON Leonid
Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School
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NAZARENO Remedios
Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School
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XIAO Sheng
Department of Pathology and Laboratory Medicine, Boston University School of Medicine
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MANN Koren
Department of Pathology and Laboratory Medicine, Boston University School of Medicine
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JARJOUR Wael
Department of Medicine, Division of Rheumatology and Immunology, University of Virginia
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MARSHAK-ROTHSTEIN Ann
Department of Microbiology, Boston University School of Medicine
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Xiao Sheng
Department Of Pathology And Laboratory Medicine Boston University School Of Medicine
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Mann Koren
Department Of Pathology And Laboratory Medicine Boston University School Of Medicine
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Jarjour Wael
Department Of Medicine Division Of Clinical Rheumatology University Of Virginia
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Jarjour Wael
Department Of Medicine Division Of Rheumatology And Immunology University Of Virginia
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Izikson Leonid
Center For Neurologic Diseases Brigham And Women's Hospital Harvard Medical School
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Nazareno Remedios
Center For Neurologic Diseases Brigham And Women's Hospital Harvard Medical School
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Marshak-rothstein Ann
Department Of Microbiology Boston University School Of Medicine
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Koldzic Djordje
Center For Neurologic Diseases Brigham And Women's Hospital Harvard Medical School
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Li Li
Department Of Cardiology Renmin Hospital Of Gansu Province
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Li Li
Department Of Cancer Epidemiology Chinese Academy Of Medical Sciences
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Li Li
Department Of Medicine Division Of Rheumatology And Immunology University Of Virginia
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JODO Satoshi
Department of Internal Medicine II, School of Medicine, Hokkaido University
著作論文
- Recovery from experimental allergic encephalomyelitis is TGF-β dependent and associated with increases in CD4^+LAP^+ and CD4^+CD25^+ T cells
- IL-10 is involved in the suppression of experimental autoimmune encephalomyelitis by CD25^+ CD4^+ regulatory T cells
- Changes in sensitivity of peripheral lymphocytes of autoimmune gld mice to FasL-mediated apoptosis reveal a mechanism for the preferential deletion of CD4^-CD8^-B220^+ T cells