Blockade of the Interaction Between PD-1 and PD-L1 Accelerates Graft Arterial Disease in Cardiac Allografts
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...
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| Veröffentlicht in: | Arteriosclerosis, thrombosis, and vascular biology thrombosis, and vascular biology, 2004-11, Vol.24 (11), p.2057-2062 |
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| creator | Koga, Noritaka Suzuki, Jun-ichi Kosuge, Hisanori Haraguchi, Go Onai, Yasuyuki Futamatsu, Hideki Maejima, Yasuhiro Gotoh, Ryo Saiki, Hitoshi Tsushima, Fumihiko Azuma, Miyuki Isobe, Mitsuaki |
| description | 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 occlusion55±5.0% versus 9.8±4.3%, P |
| doi_str_mv | 10.1161/01.ATV.0000145015.23656.e4 |
| format | Article |
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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 occlusion55±5.0% versus 9.8±4.3%, P<0.05). The expressions of interferon γ (IFN-γ) and tumor necrosis factor α of cardiac allografts were upregulated in response to anti–PD-L1 mAb treatment. In vitro, PD-L1 expression was induced in SMCs in response to IFN-γ stimulation. Sensitized splenocytes increased SMC proliferation, and anti–PD-L1 mAb in combination with IFN-γ stimulation increased this proliferation.
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.</description><identifier>ISSN: 1079-5642</identifier><identifier>EISSN: 1524-4636</identifier><identifier>DOI: 10.1161/01.ATV.0000145015.23656.e4</identifier><identifier>PMID: 15374847</identifier><identifier>CODEN: ATVBFA</identifier><language>eng</language><publisher>Philadelphia, PA: American Heart Association, Inc</publisher><subject>Animals ; Antibodies, Blocking - adverse effects ; Antibodies, Monoclonal - adverse effects ; Antigens, Surface - biosynthesis ; Antigens, Surface - immunology ; Antigens, Surface - metabolism ; Aorta - chemistry ; Aorta - cytology ; Aorta - metabolism ; Apoptosis Regulatory Proteins ; Atherosclerosis (general aspects, experimental research) ; B7-1 Antigen - biosynthesis ; B7-1 Antigen - immunology ; B7-1 Antigen - metabolism ; B7-H1 Antigen ; Biological and medical sciences ; Blood and lymphatic vessels ; Cardiology. Vascular system ; Cell Proliferation ; Cells, Cultured ; Coronary Disease - immunology ; Coronary Disease - metabolism ; Cytokines - biosynthesis ; Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous ; Graft Rejection - immunology ; Graft Rejection - metabolism ; Heart Transplantation ; Interferon-gamma - immunology ; Lymphocyte Activation - immunology ; Male ; Medical sciences ; Membrane Glycoproteins - biosynthesis ; Membrane Glycoproteins - immunology ; Membrane Glycoproteins - metabolism ; Mice ; Mice, Inbred C57BL ; Muscle, Smooth, Vascular - chemistry ; Muscle, Smooth, Vascular - cytology ; Muscle, Smooth, Vascular - metabolism ; Myocytes, Smooth Muscle - chemistry ; Myocytes, Smooth Muscle - metabolism ; Peptides - immunology ; Peptides - metabolism ; Programmed Cell Death 1 Receptor ; Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases ; Surgery of the heart ; T-Lymphocytes - metabolism ; T-Lymphocytes - physiology ; Transplantation, Homologous</subject><ispartof>Arteriosclerosis, thrombosis, and vascular biology, 2004-11, Vol.24 (11), p.2057-2062</ispartof><rights>2004 American Heart Association, Inc.</rights><rights>2005 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Nov 2004</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5723-264c3067d00f279982649020a184d89c79a79965e0f1f6b2f9d813eb09441c8e3</citedby><cites>FETCH-LOGICAL-c5723-264c3067d00f279982649020a184d89c79a79965e0f1f6b2f9d813eb09441c8e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16277090$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15374847$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Koga, Noritaka</creatorcontrib><creatorcontrib>Suzuki, Jun-ichi</creatorcontrib><creatorcontrib>Kosuge, Hisanori</creatorcontrib><creatorcontrib>Haraguchi, Go</creatorcontrib><creatorcontrib>Onai, Yasuyuki</creatorcontrib><creatorcontrib>Futamatsu, Hideki</creatorcontrib><creatorcontrib>Maejima, Yasuhiro</creatorcontrib><creatorcontrib>Gotoh, Ryo</creatorcontrib><creatorcontrib>Saiki, Hitoshi</creatorcontrib><creatorcontrib>Tsushima, Fumihiko</creatorcontrib><creatorcontrib>Azuma, Miyuki</creatorcontrib><creatorcontrib>Isobe, Mitsuaki</creatorcontrib><title>Blockade of the Interaction Between PD-1 and PD-L1 Accelerates Graft Arterial Disease in Cardiac Allografts</title><title>Arteriosclerosis, thrombosis, and vascular biology</title><addtitle>Arterioscler Thromb Vasc Biol</addtitle><description>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 occlusion55±5.0% versus 9.8±4.3%, P<0.05). The expressions of interferon γ (IFN-γ) and tumor necrosis factor α of cardiac allografts were upregulated in response to anti–PD-L1 mAb treatment. In vitro, PD-L1 expression was induced in SMCs in response to IFN-γ stimulation. Sensitized splenocytes increased SMC proliferation, and anti–PD-L1 mAb in combination with IFN-γ stimulation increased this proliferation.
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.</description><subject>Animals</subject><subject>Antibodies, Blocking - adverse effects</subject><subject>Antibodies, Monoclonal - adverse effects</subject><subject>Antigens, Surface - biosynthesis</subject><subject>Antigens, Surface - immunology</subject><subject>Antigens, Surface - metabolism</subject><subject>Aorta - chemistry</subject><subject>Aorta - cytology</subject><subject>Aorta - metabolism</subject><subject>Apoptosis Regulatory Proteins</subject><subject>Atherosclerosis (general aspects, experimental research)</subject><subject>B7-1 Antigen - biosynthesis</subject><subject>B7-1 Antigen - immunology</subject><subject>B7-1 Antigen - metabolism</subject><subject>B7-H1 Antigen</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Cardiology. Vascular system</subject><subject>Cell Proliferation</subject><subject>Cells, Cultured</subject><subject>Coronary Disease - immunology</subject><subject>Coronary Disease - metabolism</subject><subject>Cytokines - biosynthesis</subject><subject>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</subject><subject>Graft Rejection - immunology</subject><subject>Graft Rejection - metabolism</subject><subject>Heart Transplantation</subject><subject>Interferon-gamma - immunology</subject><subject>Lymphocyte Activation - immunology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Membrane Glycoproteins - biosynthesis</subject><subject>Membrane Glycoproteins - immunology</subject><subject>Membrane Glycoproteins - metabolism</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Muscle, Smooth, Vascular - chemistry</subject><subject>Muscle, Smooth, Vascular - cytology</subject><subject>Muscle, Smooth, Vascular - metabolism</subject><subject>Myocytes, Smooth Muscle - chemistry</subject><subject>Myocytes, Smooth Muscle - metabolism</subject><subject>Peptides - immunology</subject><subject>Peptides - metabolism</subject><subject>Programmed Cell Death 1 Receptor</subject><subject>Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases</subject><subject>Surgery of the heart</subject><subject>T-Lymphocytes - metabolism</subject><subject>T-Lymphocytes - physiology</subject><subject>Transplantation, Homologous</subject><issn>1079-5642</issn><issn>1524-4636</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkUFv1DAQhSMEoqXwF5BVid4SPLZjJ9zSLZRKK8GhcLW8zoRN15sUO9GKf8-EXWklfPHz6Bu_0bwsuwZeAGj4yKFoHn8WnA6okkNZCKlLXaB6kV1CKVSutNQvSXNT56VW4iJ7k9IT8UoI_jq7gFIaVSlzme1uw-h3rkU2dmzaInsYJozOT_04sFucDogD-36XA3NDu4g1sMZ7DARNmNh9dN3EmkhNvQvsrk_oErJ-YCsX29551oQw_lqo9DZ71bmQ8N3pvsp-fPn8uPqar7_dP6yade5LI2QutPKSa9Ny3glT1xUVai64g0q1Ve1N7aiqS-QddHojurqtQOKG10qBr1BeZTfHf5_j-HvGNNl9n2jk4AYc52S14UpXWhF4_R_4NM5xoNmsoFVVFS2QoE9HyMcxpYidfY793sU_Frhd8rAcLOVhz3nYf3lYXBzenxzmzR7bc-spAAI-nACXvAtddIPv05nTwhhec-LUkTuMgXaddmE-YLRbdGHaLtZKal7mggQAPfNlGCn_Agj9n80</recordid><startdate>200411</startdate><enddate>200411</enddate><creator>Koga, Noritaka</creator><creator>Suzuki, Jun-ichi</creator><creator>Kosuge, Hisanori</creator><creator>Haraguchi, Go</creator><creator>Onai, Yasuyuki</creator><creator>Futamatsu, Hideki</creator><creator>Maejima, Yasuhiro</creator><creator>Gotoh, Ryo</creator><creator>Saiki, Hitoshi</creator><creator>Tsushima, Fumihiko</creator><creator>Azuma, Miyuki</creator><creator>Isobe, Mitsuaki</creator><general>American Heart Association, Inc</general><general>Lippincott</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>K9.</scope><scope>7X8</scope></search><sort><creationdate>200411</creationdate><title>Blockade of the Interaction Between PD-1 and PD-L1 Accelerates Graft Arterial Disease in Cardiac Allografts</title><author>Koga, Noritaka ; Suzuki, Jun-ichi ; Kosuge, Hisanori ; Haraguchi, Go ; Onai, Yasuyuki ; Futamatsu, Hideki ; Maejima, Yasuhiro ; Gotoh, Ryo ; Saiki, Hitoshi ; Tsushima, Fumihiko ; Azuma, Miyuki ; Isobe, Mitsuaki</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5723-264c3067d00f279982649020a184d89c79a79965e0f1f6b2f9d813eb09441c8e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Animals</topic><topic>Antibodies, Blocking - adverse effects</topic><topic>Antibodies, Monoclonal - adverse effects</topic><topic>Antigens, Surface - biosynthesis</topic><topic>Antigens, Surface - immunology</topic><topic>Antigens, Surface - metabolism</topic><topic>Aorta - chemistry</topic><topic>Aorta - cytology</topic><topic>Aorta - metabolism</topic><topic>Apoptosis Regulatory Proteins</topic><topic>Atherosclerosis (general aspects, experimental research)</topic><topic>B7-1 Antigen - biosynthesis</topic><topic>B7-1 Antigen - immunology</topic><topic>B7-1 Antigen - metabolism</topic><topic>B7-H1 Antigen</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Cardiology. Vascular system</topic><topic>Cell Proliferation</topic><topic>Cells, Cultured</topic><topic>Coronary Disease - immunology</topic><topic>Coronary Disease - metabolism</topic><topic>Cytokines - biosynthesis</topic><topic>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</topic><topic>Graft Rejection - immunology</topic><topic>Graft Rejection - metabolism</topic><topic>Heart Transplantation</topic><topic>Interferon-gamma - immunology</topic><topic>Lymphocyte Activation - immunology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Membrane Glycoproteins - biosynthesis</topic><topic>Membrane Glycoproteins - immunology</topic><topic>Membrane Glycoproteins - metabolism</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Muscle, Smooth, Vascular - chemistry</topic><topic>Muscle, Smooth, Vascular - cytology</topic><topic>Muscle, Smooth, Vascular - metabolism</topic><topic>Myocytes, Smooth Muscle - chemistry</topic><topic>Myocytes, Smooth Muscle - metabolism</topic><topic>Peptides - immunology</topic><topic>Peptides - metabolism</topic><topic>Programmed Cell Death 1 Receptor</topic><topic>Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases</topic><topic>Surgery of the heart</topic><topic>T-Lymphocytes - metabolism</topic><topic>T-Lymphocytes - physiology</topic><topic>Transplantation, Homologous</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Koga, Noritaka</creatorcontrib><creatorcontrib>Suzuki, Jun-ichi</creatorcontrib><creatorcontrib>Kosuge, Hisanori</creatorcontrib><creatorcontrib>Haraguchi, Go</creatorcontrib><creatorcontrib>Onai, Yasuyuki</creatorcontrib><creatorcontrib>Futamatsu, Hideki</creatorcontrib><creatorcontrib>Maejima, Yasuhiro</creatorcontrib><creatorcontrib>Gotoh, Ryo</creatorcontrib><creatorcontrib>Saiki, Hitoshi</creatorcontrib><creatorcontrib>Tsushima, Fumihiko</creatorcontrib><creatorcontrib>Azuma, Miyuki</creatorcontrib><creatorcontrib>Isobe, Mitsuaki</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Arteriosclerosis, thrombosis, and vascular biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Koga, Noritaka</au><au>Suzuki, Jun-ichi</au><au>Kosuge, Hisanori</au><au>Haraguchi, Go</au><au>Onai, Yasuyuki</au><au>Futamatsu, Hideki</au><au>Maejima, Yasuhiro</au><au>Gotoh, Ryo</au><au>Saiki, Hitoshi</au><au>Tsushima, Fumihiko</au><au>Azuma, Miyuki</au><au>Isobe, Mitsuaki</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Blockade of the Interaction Between PD-1 and PD-L1 Accelerates Graft Arterial Disease in Cardiac Allografts</atitle><jtitle>Arteriosclerosis, thrombosis, and vascular biology</jtitle><addtitle>Arterioscler Thromb Vasc Biol</addtitle><date>2004-11</date><risdate>2004</risdate><volume>24</volume><issue>11</issue><spage>2057</spage><epage>2062</epage><pages>2057-2062</pages><issn>1079-5642</issn><eissn>1524-4636</eissn><coden>ATVBFA</coden><abstract>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 occlusion55±5.0% versus 9.8±4.3%, P<0.05). The expressions of interferon γ (IFN-γ) and tumor necrosis factor α of cardiac allografts were upregulated in response to anti–PD-L1 mAb treatment. In vitro, PD-L1 expression was induced in SMCs in response to IFN-γ stimulation. Sensitized splenocytes increased SMC proliferation, and anti–PD-L1 mAb in combination with IFN-γ stimulation increased this proliferation.
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.</abstract><cop>Philadelphia, PA</cop><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>15374847</pmid><doi>10.1161/01.ATV.0000145015.23656.e4</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 1079-5642 |
| ispartof | Arteriosclerosis, thrombosis, and vascular biology, 2004-11, Vol.24 (11), p.2057-2062 |
| issn | 1079-5642 1524-4636 |
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| source | MEDLINE; Journals@Ovid Complete; Alma/SFX Local Collection |
| subjects | Animals Antibodies, Blocking - adverse effects Antibodies, Monoclonal - adverse effects Antigens, Surface - biosynthesis Antigens, Surface - immunology Antigens, Surface - metabolism Aorta - chemistry Aorta - cytology Aorta - metabolism Apoptosis Regulatory Proteins Atherosclerosis (general aspects, experimental research) B7-1 Antigen - biosynthesis B7-1 Antigen - immunology B7-1 Antigen - metabolism B7-H1 Antigen Biological and medical sciences Blood and lymphatic vessels Cardiology. Vascular system Cell Proliferation Cells, Cultured Coronary Disease - immunology Coronary Disease - metabolism Cytokines - biosynthesis Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous Graft Rejection - immunology Graft Rejection - metabolism Heart Transplantation Interferon-gamma - immunology Lymphocyte Activation - immunology Male Medical sciences Membrane Glycoproteins - biosynthesis Membrane Glycoproteins - immunology Membrane Glycoproteins - metabolism Mice Mice, Inbred C57BL Muscle, Smooth, Vascular - chemistry Muscle, Smooth, Vascular - cytology Muscle, Smooth, Vascular - metabolism Myocytes, Smooth Muscle - chemistry Myocytes, Smooth Muscle - metabolism Peptides - immunology Peptides - metabolism Programmed Cell Death 1 Receptor Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases Surgery of the heart T-Lymphocytes - metabolism T-Lymphocytes - physiology Transplantation, Homologous |
| title | Blockade of the Interaction Between PD-1 and PD-L1 Accelerates Graft Arterial Disease in Cardiac Allografts |
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