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- Mary E. Keir
- Department of Pathology, Harvard Medical School and Brigham and Women's Hospital, Boston, Massachusetts 02115-5727;
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- Manish J. Butte
- Department of Pathology, Harvard Medical School and Brigham and Women's Hospital, Boston, Massachusetts 02115-5727;
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- Gordon J. Freeman
- Department of Medical Oncology, Dana Farber Cancer Institute, Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115-6013
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- Arlene H. Sharpe
- Department of Pathology, Harvard Medical School and Brigham and Women's Hospital, Boston, Massachusetts 02115-5727;
説明
<jats:p>Programmed death 1 (PD-1) and its ligands, PD-L1 and PD-L2, deliver inhibitory signals that regulate the balance between T cell activation, tolerance, and immunopathology. Immune responses to foreign and self-antigens require specific and balanced responses to clear pathogens and tumors and yet maintain tolerance. Induction and maintenance of T cell tolerance requires PD-1, and its ligand PD-L1 on nonhematopoietic cells can limit effector T cell responses and protect tissues from immune-mediated tissue damage. The PD-1:PD-L pathway also has been usurped by microorganisms and tumors to attenuate antimicrobial or tumor immunity and facilitate chronic infection and tumor survival. The identification of B7-1 as an additional binding partner for PD-L1, together with the discovery of an inhibitory bidirectional interaction between PD-L1 and B7-1, reveals new ways the B7:CD28 family regulates T cell activation and tolerance. In this review, we discuss current understanding of the immunoregulatory functions of PD-1 and its ligands and their therapeutic potential.</jats:p>
収録刊行物
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- Annual Review of Immunology
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Annual Review of Immunology 26 (1), 677-704, 2008-04-01
Annual Reviews
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詳細情報 詳細情報について
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- CRID
- 1360574094677043584
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- ISSN
- 15453278
- 07320582
- http://id.crossref.org/issn/07320582
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- データソース種別
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- Crossref