Immune Escape for Renal Cell Carcinoma: CD70 Mediates Apoptosis in Lymphocytes
Tumors can escape immune recognition and destruction through the induction of apoptosis in lymphocytes. Although renal cell carcinoma (RCC) is able to prevent immune recognition, only a few genes (such as FasL) that are relevant for RCC immune escape have been identified so far. We have previously s...
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| Veröffentlicht in: | Neoplasia (New York, N.Y.) N.Y.), 2006-11, Vol.8 (11), p.933-938 |
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| container_title | Neoplasia (New York, N.Y.) |
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| creator | Diegmann, Julia Junker, Kerstin Loncarevic, Ivan F. Michel, Susanne Schimmel, Bettina von Eagelinq, Ferdinand |
| description | Tumors can escape immune recognition and destruction through the induction of apoptosis in lymphocytes. Although renal cell carcinoma (RCC) is able to prevent immune recognition, only a few genes (such as FasL) that are relevant for RCC immune escape have been identified so far. We have previously shown that some apoptosis-inducing genes are overexpressed in RCC. We hypothesized that these genes could be part of the immune-escape strategy of these tumors. Here we report that CD70, a cytokine overexpressed in RCC, promotes lymphocyte apoptosis through interaction with its receptor CD27 and with the intracellular receptor-binding protein SIVA. Apoptosis increased after cocultivating lymphocytes with the RCC cell lines A498 and CAKI2. The addition of recombinant soluble CD70 to both native lymphocytes and a T-cell cell line resulted in increased lymphocyte apoptosis as well. Furthermore, induced apoptosis could be partially blocked with anti-CD27 and anti-CD70 antibodies. Our results strongly indicate a role for CD70 and CD27 receptor in lymphocyte apoptosis within the tumor environment. Apoptosis mediated by exposure to the CD70 secreted by tumor cells may contribute to the failure of RCC patients to develop an effective lymphocyte-mediated antitumor response. |
| doi_str_mv | 10.1593/neo.06451 |
| format | Article |
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Although renal cell carcinoma (RCC) is able to prevent immune recognition, only a few genes (such as FasL) that are relevant for RCC immune escape have been identified so far. We have previously shown that some apoptosis-inducing genes are overexpressed in RCC. We hypothesized that these genes could be part of the immune-escape strategy of these tumors. Here we report that CD70, a cytokine overexpressed in RCC, promotes lymphocyte apoptosis through interaction with its receptor CD27 and with the intracellular receptor-binding protein SIVA. Apoptosis increased after cocultivating lymphocytes with the RCC cell lines A498 and CAKI2. The addition of recombinant soluble CD70 to both native lymphocytes and a T-cell cell line resulted in increased lymphocyte apoptosis as well. Furthermore, induced apoptosis could be partially blocked with anti-CD27 and anti-CD70 antibodies. Our results strongly indicate a role for CD70 and CD27 receptor in lymphocyte apoptosis within the tumor environment. Apoptosis mediated by exposure to the CD70 secreted by tumor cells may contribute to the failure of RCC patients to develop an effective lymphocyte-mediated antitumor response.</description><identifier>ISSN: 1476-5586</identifier><identifier>ISSN: 1522-8002</identifier><identifier>EISSN: 1476-5586</identifier><identifier>EISSN: 1522-8002</identifier><identifier>DOI: 10.1593/neo.06451</identifier><identifier>PMID: 17132225</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Apoptosis ; Carcinoma, Renal Cell - blood ; Carcinoma, Renal Cell - immunology ; CD27 ; CD27 Ligand - biosynthesis ; Cell Line, Tumor ; Gene Expression Regulation, Neoplastic ; Humans ; immune suppression ; Immune System ; Kidney ; Kidney Neoplasms - blood ; Kidney Neoplasms - immunology ; Lymphocyte Activation ; Lymphocytes - metabolism ; Lymphocytes - pathology ; Membrane Proteins - chemistry ; Models, Biological ; SIVA ; TNFSF7 ; Tumor Necrosis Factor Receptor Superfamily, Member 7 - biosynthesis</subject><ispartof>Neoplasia (New York, N.Y.), 2006-11, Vol.8 (11), p.933-938</ispartof><rights>2006 Neoplasia Press, Inc.</rights><rights>Copyright © 2006 Neoplasia Press, Inc. 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Although renal cell carcinoma (RCC) is able to prevent immune recognition, only a few genes (such as FasL) that are relevant for RCC immune escape have been identified so far. We have previously shown that some apoptosis-inducing genes are overexpressed in RCC. We hypothesized that these genes could be part of the immune-escape strategy of these tumors. Here we report that CD70, a cytokine overexpressed in RCC, promotes lymphocyte apoptosis through interaction with its receptor CD27 and with the intracellular receptor-binding protein SIVA. Apoptosis increased after cocultivating lymphocytes with the RCC cell lines A498 and CAKI2. The addition of recombinant soluble CD70 to both native lymphocytes and a T-cell cell line resulted in increased lymphocyte apoptosis as well. Furthermore, induced apoptosis could be partially blocked with anti-CD27 and anti-CD70 antibodies. Our results strongly indicate a role for CD70 and CD27 receptor in lymphocyte apoptosis within the tumor environment. Apoptosis mediated by exposure to the CD70 secreted by tumor cells may contribute to the failure of RCC patients to develop an effective lymphocyte-mediated antitumor response.</description><subject>Apoptosis</subject><subject>Carcinoma, Renal Cell - blood</subject><subject>Carcinoma, Renal Cell - immunology</subject><subject>CD27</subject><subject>CD27 Ligand - biosynthesis</subject><subject>Cell Line, Tumor</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humans</subject><subject>immune suppression</subject><subject>Immune System</subject><subject>Kidney</subject><subject>Kidney Neoplasms - blood</subject><subject>Kidney Neoplasms - immunology</subject><subject>Lymphocyte Activation</subject><subject>Lymphocytes - metabolism</subject><subject>Lymphocytes - pathology</subject><subject>Membrane Proteins - chemistry</subject><subject>Models, Biological</subject><subject>SIVA</subject><subject>TNFSF7</subject><subject>Tumor Necrosis Factor Receptor Superfamily, Member 7 - biosynthesis</subject><issn>1476-5586</issn><issn>1522-8002</issn><issn>1476-5586</issn><issn>1522-8002</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>DOA</sourceid><recordid>eNqFkV1rFDEUhgdRbK1e-AdkrgQvtuZMviZeCGVt68KqIHodziRn2pSdyZjMFvbfm3YXbUHwJgk5T54czltVr4GdgjT8_UjxlCkh4Ul1DEKrhZStevrgfFS9yPmGMVCg9fPqCDTwpmnkcfV1NQzbkerz7HCiuo-p_k4jbuolbcqCyYUxDvihXn7SrP5CPuBMuT6b4jTHHHIdxnq9G6br6Hal8LJ61uMm06vDflL9vDj_sfy8WH-7XC3P1gsnQcwLaE3bC9QAyGUngDvQjFTruRPQKOWZ57KlxpP3je7I9cJ1zrTK9F2vOfKTarX3-og3dkphwLSzEYO9v4jpymKag9uQNVI5MgiGjBfY9lg-4UobpzoSEpvi-rh3TdtuIO9onBNuHkkfV8Zwba_irS1TVAzuBG8PghR_bSnPdgjZlflhCWabrWrB6Fb_H2yYYI1RuoDv9qBLMedE_Z9ugNm7yG15YO8jL-ybh-3_JQ8ZF4DvASqB3AZKNrtAoytZJnJzmVj4h_Y3mSu4zA</recordid><startdate>20061101</startdate><enddate>20061101</enddate><creator>Diegmann, Julia</creator><creator>Junker, Kerstin</creator><creator>Loncarevic, Ivan F.</creator><creator>Michel, Susanne</creator><creator>Schimmel, Bettina</creator><creator>von Eagelinq, Ferdinand</creator><general>Elsevier Inc</general><general>Neoplasia Press Inc</general><general>Elsevier</general><scope>6I.</scope><scope>AAFTH</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>7T5</scope><scope>H94</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20061101</creationdate><title>Immune Escape for Renal Cell Carcinoma: CD70 Mediates Apoptosis in Lymphocytes</title><author>Diegmann, Julia ; Junker, Kerstin ; Loncarevic, Ivan F. ; Michel, Susanne ; Schimmel, Bettina ; von Eagelinq, Ferdinand</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c514t-1898f4a711a35b413c170e68d3c41266d0d358e2dedd27becf4cbc9869fbf73a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Apoptosis</topic><topic>Carcinoma, Renal Cell - blood</topic><topic>Carcinoma, Renal Cell - immunology</topic><topic>CD27</topic><topic>CD27 Ligand - biosynthesis</topic><topic>Cell Line, Tumor</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Humans</topic><topic>immune suppression</topic><topic>Immune System</topic><topic>Kidney</topic><topic>Kidney Neoplasms - blood</topic><topic>Kidney Neoplasms - immunology</topic><topic>Lymphocyte Activation</topic><topic>Lymphocytes - metabolism</topic><topic>Lymphocytes - pathology</topic><topic>Membrane Proteins - chemistry</topic><topic>Models, Biological</topic><topic>SIVA</topic><topic>TNFSF7</topic><topic>Tumor Necrosis Factor Receptor Superfamily, Member 7 - biosynthesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Diegmann, Julia</creatorcontrib><creatorcontrib>Junker, Kerstin</creatorcontrib><creatorcontrib>Loncarevic, Ivan F.</creatorcontrib><creatorcontrib>Michel, Susanne</creatorcontrib><creatorcontrib>Schimmel, Bettina</creatorcontrib><creatorcontrib>von Eagelinq, Ferdinand</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Neoplasia (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Diegmann, Julia</au><au>Junker, Kerstin</au><au>Loncarevic, Ivan F.</au><au>Michel, Susanne</au><au>Schimmel, Bettina</au><au>von Eagelinq, Ferdinand</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Immune Escape for Renal Cell Carcinoma: CD70 Mediates Apoptosis in Lymphocytes</atitle><jtitle>Neoplasia (New York, N.Y.)</jtitle><addtitle>Neoplasia</addtitle><date>2006-11-01</date><risdate>2006</risdate><volume>8</volume><issue>11</issue><spage>933</spage><epage>938</epage><pages>933-938</pages><issn>1476-5586</issn><issn>1522-8002</issn><eissn>1476-5586</eissn><eissn>1522-8002</eissn><abstract>Tumors can escape immune recognition and destruction through the induction of apoptosis in lymphocytes. Although renal cell carcinoma (RCC) is able to prevent immune recognition, only a few genes (such as FasL) that are relevant for RCC immune escape have been identified so far. We have previously shown that some apoptosis-inducing genes are overexpressed in RCC. We hypothesized that these genes could be part of the immune-escape strategy of these tumors. Here we report that CD70, a cytokine overexpressed in RCC, promotes lymphocyte apoptosis through interaction with its receptor CD27 and with the intracellular receptor-binding protein SIVA. Apoptosis increased after cocultivating lymphocytes with the RCC cell lines A498 and CAKI2. The addition of recombinant soluble CD70 to both native lymphocytes and a T-cell cell line resulted in increased lymphocyte apoptosis as well. Furthermore, induced apoptosis could be partially blocked with anti-CD27 and anti-CD70 antibodies. Our results strongly indicate a role for CD70 and CD27 receptor in lymphocyte apoptosis within the tumor environment. Apoptosis mediated by exposure to the CD70 secreted by tumor cells may contribute to the failure of RCC patients to develop an effective lymphocyte-mediated antitumor response.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>17132225</pmid><doi>10.1593/neo.06451</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Apoptosis Carcinoma, Renal Cell - blood Carcinoma, Renal Cell - immunology CD27 CD27 Ligand - biosynthesis Cell Line, Tumor Gene Expression Regulation, Neoplastic Humans immune suppression Immune System Kidney Kidney Neoplasms - blood Kidney Neoplasms - immunology Lymphocyte Activation Lymphocytes - metabolism Lymphocytes - pathology Membrane Proteins - chemistry Models, Biological SIVA TNFSF7 Tumor Necrosis Factor Receptor Superfamily, Member 7 - biosynthesis |
| title | Immune Escape for Renal Cell Carcinoma: CD70 Mediates Apoptosis in Lymphocytes |
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