Blockade of the Interaction Between PD-1 and PD-L1 Accelerates Graft Arterial Disease in Cardiac Allografts
| Autor: | Ryo Gotoh, Yasuyuki Onai, Yasuhiro Maejima, Miyuki Azuma, Hisanori Kosuge, Hideki Futamatsu, Mitsuaki Isobe, Go Haraguchi, Jun-ichi Suzuki, Noritaka Koga, Hitoshi Saiki, Fumihiko Tsushima |
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| Rok vydání: | 2004 |
| Předmět: |
Graft Rejection
Male Pathology medicine.medical_specialty T-Lymphocytes medicine.medical_treatment Myocytes Smooth Muscle Programmed Cell Death 1 Receptor Coronary Disease Lymphocyte Activation B7-H1 Antigen Muscle Smooth Vascular Interferon-gamma Mice Immune system PD-L1 medicine Animals Transplantation Homologous Myocyte Antibodies Blocking Aorta Cells Cultured Cell Proliferation Heart transplantation Membrane Glycoproteins biology business.industry Vascular disease Antibodies Monoclonal medicine.disease Blockade Mice Inbred C57BL Transplantation Coronary arteries medicine.anatomical_structure Antigens Surface Immunology B7-1 Antigen biology.protein Cytokines Heart Transplantation Apoptosis Regulatory Proteins Peptides Cardiology and Cardiovascular Medicine business |
| Zdroj: | Arteriosclerosis, Thrombosis, and Vascular Biology. 24:2057-2062 |
| ISSN: | 1524-4636 1079-5642 |
| Popis: | Background— Programmed death-1 (PD-1), a member of the CD28 family, has been identified. PD-1 is involved in the negative regulation of some immune responses. We evaluated the role of PD-ligand 1 (PD-L1) in graft arterial disease (GAD) of cardiac allografts and in smooth muscle cells (SMCs). Methods and Results— C57BL/6 murine hearts were transplanted into B6.C-H2KhEg mice for examination of GAD. PD-L1 was expressed in SMCs of the thickened intima in the graft coronary arteries, and administration of anti–PD-L1 monoclonal antibody (mAb) enhanced the progression of GAD (luminal occlusion: 55±5.0% versus 9.8±4.3%, P Conclusions— The PD-L1 pathway regulates both the proliferation of SMCs and GAD. Thus, control of this interaction is a promising strategy for suppression of GAD. |
| Databáze: | OpenAIRE |
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