The Contribution of Vascular Endothelial Growth Factor to the Induction of Regulatory T-Cells in Malignant Effusions
It has been suggested that immunosuppressive cytokines such as transforming growth factor β (TGF-β) and interleukin 10 play an important role in the induction and/or maintenance of regulatory T-cells (Tregs) in patients with cancer. In the present study, whether or not vascular endothelial growth...
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| Veröffentlicht in: | Anticancer research 2009-03, Vol.29 (3), p.881-888 |
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| creator | WADA, Junji SUZUKI, Hiroyuki KATANO, Mitsuo FUCHINO, Ryouta YAMASAKI, Akio NAGAI, Shuntaro YANAI, Kousuke KOGA, Kenichiro NAKAMURA, Masafumi TANAKA, Masao MORISAKI, Takashi |
| description | It has been suggested that immunosuppressive cytokines such as transforming growth factor β (TGF-β) and interleukin 10 play
an important role in the induction and/or maintenance of regulatory T-cells (Tregs) in patients with cancer. In the present
study, whether or not vascular endothelial growth factor (VEGF) contributes to the induction and/or maintenance of Tregs was
examined, because of experience with a patient in whom a positive correlation between VEGF concentration and the percentage
of Tregs (% Tregs) among the total CD4 + T-cells in the pleural effusion was found during dendritic cell activated lymphocyte therapy. CD4 + CD25 high T-cells were estimated as Tregs in the present study. In an in vitro experimental system, VEGF-containing malignant effusions
increased the % Tregs in autologous peripheral blood mononuclear cells (PBMCs), which could be suppressed by the addition
of a humanized monoclonal anti-VEGF antibody (bevacizumab [Avastin]). When VEGF-producing hepatic carcinoma cells were mix-cultured
with PBMCs, the % Tregs increased and this increase was also suppressed by the addition of bevacizumab. Whether or not bevacizumab
can affect the % Tregs of PBMCs in patients with colon cancer was also examined. Three out of four patients showed a significant
decrease of the % Tregs after intravenous injection of bevacizumab. Interestingly, the expression of VEGF receptor-2 (VEGFR-2)
was higher in Tregs than in other CD4 + T-cells. Taken together, the data presented here indicate a contribution of VEGF to induction and/or maintenance of Tregs
in patients with cancer. |
| format | Article |
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an important role in the induction and/or maintenance of regulatory T-cells (Tregs) in patients with cancer. In the present
study, whether or not vascular endothelial growth factor (VEGF) contributes to the induction and/or maintenance of Tregs was
examined, because of experience with a patient in whom a positive correlation between VEGF concentration and the percentage
of Tregs (% Tregs) among the total CD4 + T-cells in the pleural effusion was found during dendritic cell activated lymphocyte therapy. CD4 + CD25 high T-cells were estimated as Tregs in the present study. In an in vitro experimental system, VEGF-containing malignant effusions
increased the % Tregs in autologous peripheral blood mononuclear cells (PBMCs), which could be suppressed by the addition
of a humanized monoclonal anti-VEGF antibody (bevacizumab [Avastin]). When VEGF-producing hepatic carcinoma cells were mix-cultured
with PBMCs, the % Tregs increased and this increase was also suppressed by the addition of bevacizumab. Whether or not bevacizumab
can affect the % Tregs of PBMCs in patients with colon cancer was also examined. Three out of four patients showed a significant
decrease of the % Tregs after intravenous injection of bevacizumab. Interestingly, the expression of VEGF receptor-2 (VEGFR-2)
was higher in Tregs than in other CD4 + T-cells. Taken together, the data presented here indicate a contribution of VEGF to induction and/or maintenance of Tregs
in patients with cancer.</description><identifier>ISSN: 0250-7005</identifier><identifier>EISSN: 1791-7530</identifier><identifier>PMID: 19414323</identifier><language>eng</language><publisher>Attiki: International Institute of Anticancer Research</publisher><subject>Adult ; Aged ; Angiogenesis Inhibitors - therapeutic use ; Antibodies, Monoclonal - therapeutic use ; Antibodies, Monoclonal, Humanized ; Bevacizumab ; Biological and medical sciences ; Dendritic Cells - transplantation ; Enzyme-Linked Immunosorbent Assay ; Female ; Flow Cytometry ; Humans ; Immunotherapy ; Male ; Medical sciences ; Middle Aged ; Neoplasms - immunology ; Neoplasms - therapy ; Pleural Effusion, Malignant - immunology ; Pleural Effusion, Malignant - therapy ; T-Lymphocytes, Regulatory - immunology ; Tumors ; Vaccination ; Vascular Endothelial Growth Factor A - antagonists & inhibitors ; Vascular Endothelial Growth Factor A - physiology ; Vascular Endothelial Growth Factor Receptor-2 - metabolism</subject><ispartof>Anticancer research, 2009-03, Vol.29 (3), p.881-888</ispartof><rights>2009 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>309,310,314,780,784,789,790,23930,23931,25140</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21515399$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19414323$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>WADA, Junji</creatorcontrib><creatorcontrib>SUZUKI, Hiroyuki</creatorcontrib><creatorcontrib>KATANO, Mitsuo</creatorcontrib><creatorcontrib>FUCHINO, Ryouta</creatorcontrib><creatorcontrib>YAMASAKI, Akio</creatorcontrib><creatorcontrib>NAGAI, Shuntaro</creatorcontrib><creatorcontrib>YANAI, Kousuke</creatorcontrib><creatorcontrib>KOGA, Kenichiro</creatorcontrib><creatorcontrib>NAKAMURA, Masafumi</creatorcontrib><creatorcontrib>TANAKA, Masao</creatorcontrib><creatorcontrib>MORISAKI, Takashi</creatorcontrib><title>The Contribution of Vascular Endothelial Growth Factor to the Induction of Regulatory T-Cells in Malignant Effusions</title><title>Anticancer research</title><addtitle>Anticancer Res</addtitle><description>It has been suggested that immunosuppressive cytokines such as transforming growth factor β (TGF-β) and interleukin 10 play
an important role in the induction and/or maintenance of regulatory T-cells (Tregs) in patients with cancer. In the present
study, whether or not vascular endothelial growth factor (VEGF) contributes to the induction and/or maintenance of Tregs was
examined, because of experience with a patient in whom a positive correlation between VEGF concentration and the percentage
of Tregs (% Tregs) among the total CD4 + T-cells in the pleural effusion was found during dendritic cell activated lymphocyte therapy. CD4 + CD25 high T-cells were estimated as Tregs in the present study. In an in vitro experimental system, VEGF-containing malignant effusions
increased the % Tregs in autologous peripheral blood mononuclear cells (PBMCs), which could be suppressed by the addition
of a humanized monoclonal anti-VEGF antibody (bevacizumab [Avastin]). When VEGF-producing hepatic carcinoma cells were mix-cultured
with PBMCs, the % Tregs increased and this increase was also suppressed by the addition of bevacizumab. Whether or not bevacizumab
can affect the % Tregs of PBMCs in patients with colon cancer was also examined. Three out of four patients showed a significant
decrease of the % Tregs after intravenous injection of bevacizumab. Interestingly, the expression of VEGF receptor-2 (VEGFR-2)
was higher in Tregs than in other CD4 + T-cells. Taken together, the data presented here indicate a contribution of VEGF to induction and/or maintenance of Tregs
in patients with cancer.</description><subject>Adult</subject><subject>Aged</subject><subject>Angiogenesis Inhibitors - therapeutic use</subject><subject>Antibodies, Monoclonal - therapeutic use</subject><subject>Antibodies, Monoclonal, Humanized</subject><subject>Bevacizumab</subject><subject>Biological and medical sciences</subject><subject>Dendritic Cells - transplantation</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Female</subject><subject>Flow Cytometry</subject><subject>Humans</subject><subject>Immunotherapy</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Neoplasms - immunology</subject><subject>Neoplasms - therapy</subject><subject>Pleural Effusion, Malignant - immunology</subject><subject>Pleural Effusion, Malignant - therapy</subject><subject>T-Lymphocytes, Regulatory - immunology</subject><subject>Tumors</subject><subject>Vaccination</subject><subject>Vascular Endothelial Growth Factor A - antagonists & inhibitors</subject><subject>Vascular Endothelial Growth Factor A - physiology</subject><subject>Vascular Endothelial Growth Factor Receptor-2 - metabolism</subject><issn>0250-7005</issn><issn>1791-7530</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkF1LwzAYhYsobk7_guRCvSvko2mbSynbHEwEmd6WNE3XSJrMJGXs3xvZ5q1XLy_nOYfDuUimqGAoLSiBl8kUYgrTAkI6SW68_4Iwz1lJrpMJYhnKCCbTJGx6CSprglPNGJQ1wHbgk3sxau7A3LQ29FIrrsHS2X3owYKLYB0IFkQBrEw7irPtXW6jK6oHsEkrqbUHyoBXrtXWcBPAvOtGH1l_m1x1XHt5d7qz5GMx31Qv6fptuaqe12mPGQspaihsqGBIEpJT2BLeiBKVWVPgsmQtQjAXhHLc5vGjrUQEU0SLUtCMQIwZmSVPx9yds9-j9KEelBexGDfSjr7OC8TKEuX_ghiiDGFEI3h_AsdmkG29c2rg7lCfB43A4wmIG3LdOW6E8n9czIgp7Lfaw5Hr1bbfKydrP3CtYyypucOsJnVsRn4AWSmLXg</recordid><startdate>20090301</startdate><enddate>20090301</enddate><creator>WADA, Junji</creator><creator>SUZUKI, Hiroyuki</creator><creator>KATANO, Mitsuo</creator><creator>FUCHINO, Ryouta</creator><creator>YAMASAKI, Akio</creator><creator>NAGAI, Shuntaro</creator><creator>YANAI, Kousuke</creator><creator>KOGA, Kenichiro</creator><creator>NAKAMURA, Masafumi</creator><creator>TANAKA, Masao</creator><creator>MORISAKI, Takashi</creator><general>International Institute of Anticancer Research</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7T5</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>20090301</creationdate><title>The Contribution of Vascular Endothelial Growth Factor to the Induction of Regulatory T-Cells in Malignant Effusions</title><author>WADA, Junji ; SUZUKI, Hiroyuki ; KATANO, Mitsuo ; FUCHINO, Ryouta ; YAMASAKI, Akio ; NAGAI, Shuntaro ; YANAI, Kousuke ; KOGA, Kenichiro ; NAKAMURA, Masafumi ; TANAKA, Masao ; MORISAKI, Takashi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h299t-1b50b5c91e33650d3abc8184b72889d1106c35a2d689d5de13251578c54302293</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Angiogenesis Inhibitors - therapeutic use</topic><topic>Antibodies, Monoclonal - therapeutic use</topic><topic>Antibodies, Monoclonal, Humanized</topic><topic>Bevacizumab</topic><topic>Biological and medical sciences</topic><topic>Dendritic Cells - transplantation</topic><topic>Enzyme-Linked Immunosorbent Assay</topic><topic>Female</topic><topic>Flow Cytometry</topic><topic>Humans</topic><topic>Immunotherapy</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Neoplasms - immunology</topic><topic>Neoplasms - therapy</topic><topic>Pleural Effusion, Malignant - immunology</topic><topic>Pleural Effusion, Malignant - therapy</topic><topic>T-Lymphocytes, Regulatory - immunology</topic><topic>Tumors</topic><topic>Vaccination</topic><topic>Vascular Endothelial Growth Factor A - antagonists & inhibitors</topic><topic>Vascular Endothelial Growth Factor A - physiology</topic><topic>Vascular Endothelial Growth Factor Receptor-2 - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>WADA, Junji</creatorcontrib><creatorcontrib>SUZUKI, Hiroyuki</creatorcontrib><creatorcontrib>KATANO, Mitsuo</creatorcontrib><creatorcontrib>FUCHINO, Ryouta</creatorcontrib><creatorcontrib>YAMASAKI, Akio</creatorcontrib><creatorcontrib>NAGAI, Shuntaro</creatorcontrib><creatorcontrib>YANAI, Kousuke</creatorcontrib><creatorcontrib>KOGA, Kenichiro</creatorcontrib><creatorcontrib>NAKAMURA, Masafumi</creatorcontrib><creatorcontrib>TANAKA, Masao</creatorcontrib><creatorcontrib>MORISAKI, Takashi</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>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Anticancer research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>WADA, Junji</au><au>SUZUKI, Hiroyuki</au><au>KATANO, Mitsuo</au><au>FUCHINO, Ryouta</au><au>YAMASAKI, Akio</au><au>NAGAI, Shuntaro</au><au>YANAI, Kousuke</au><au>KOGA, Kenichiro</au><au>NAKAMURA, Masafumi</au><au>TANAKA, Masao</au><au>MORISAKI, Takashi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Contribution of Vascular Endothelial Growth Factor to the Induction of Regulatory T-Cells in Malignant Effusions</atitle><jtitle>Anticancer research</jtitle><addtitle>Anticancer Res</addtitle><date>2009-03-01</date><risdate>2009</risdate><volume>29</volume><issue>3</issue><spage>881</spage><epage>888</epage><pages>881-888</pages><issn>0250-7005</issn><eissn>1791-7530</eissn><abstract>It has been suggested that immunosuppressive cytokines such as transforming growth factor β (TGF-β) and interleukin 10 play
an important role in the induction and/or maintenance of regulatory T-cells (Tregs) in patients with cancer. In the present
study, whether or not vascular endothelial growth factor (VEGF) contributes to the induction and/or maintenance of Tregs was
examined, because of experience with a patient in whom a positive correlation between VEGF concentration and the percentage
of Tregs (% Tregs) among the total CD4 + T-cells in the pleural effusion was found during dendritic cell activated lymphocyte therapy. CD4 + CD25 high T-cells were estimated as Tregs in the present study. In an in vitro experimental system, VEGF-containing malignant effusions
increased the % Tregs in autologous peripheral blood mononuclear cells (PBMCs), which could be suppressed by the addition
of a humanized monoclonal anti-VEGF antibody (bevacizumab [Avastin]). When VEGF-producing hepatic carcinoma cells were mix-cultured
with PBMCs, the % Tregs increased and this increase was also suppressed by the addition of bevacizumab. Whether or not bevacizumab
can affect the % Tregs of PBMCs in patients with colon cancer was also examined. Three out of four patients showed a significant
decrease of the % Tregs after intravenous injection of bevacizumab. Interestingly, the expression of VEGF receptor-2 (VEGFR-2)
was higher in Tregs than in other CD4 + T-cells. Taken together, the data presented here indicate a contribution of VEGF to induction and/or maintenance of Tregs
in patients with cancer.</abstract><cop>Attiki</cop><pub>International Institute of Anticancer Research</pub><pmid>19414323</pmid><tpages>8</tpages></addata></record> |
| fulltext | fulltext |
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| ispartof | Anticancer research, 2009-03, Vol.29 (3), p.881-888 |
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| language | eng |
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| source | MEDLINE; EZB-FREE-00999 freely available EZB journals |
| subjects | Adult Aged Angiogenesis Inhibitors - therapeutic use Antibodies, Monoclonal - therapeutic use Antibodies, Monoclonal, Humanized Bevacizumab Biological and medical sciences Dendritic Cells - transplantation Enzyme-Linked Immunosorbent Assay Female Flow Cytometry Humans Immunotherapy Male Medical sciences Middle Aged Neoplasms - immunology Neoplasms - therapy Pleural Effusion, Malignant - immunology Pleural Effusion, Malignant - therapy T-Lymphocytes, Regulatory - immunology Tumors Vaccination Vascular Endothelial Growth Factor A - antagonists & inhibitors Vascular Endothelial Growth Factor A - physiology Vascular Endothelial Growth Factor Receptor-2 - metabolism |
| title | The Contribution of Vascular Endothelial Growth Factor to the Induction of Regulatory T-Cells in Malignant Effusions |
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