Preferential migration of regulatory T cells mediated by glioma-secreted chemokines can be blocked with chemotherapy
Despite the immunogenicity of glioblastoma multiforme (GBM), immune-mediated eradication of these tumors remains deficient. Regulatory T cells (Tregs) in the blood and within the tumor microenvironment of GBM patients are known to contribute to their dismal immune responses. Here, we determined whic...
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| Veröffentlicht in: | Cancer Immunology, Immunotherapy Immunotherapy, 2008-01, Vol.57 (1), p.123-131 |
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| creator | Jordan, Justin T. Sun, Wei Hussain, S. Farzana DeAngulo, Guillermo Prabhu, Sujit S. Heimberger, Amy B. |
| description | Despite the immunogenicity of glioblastoma multiforme (GBM), immune-mediated eradication of these tumors remains deficient. Regulatory T cells (Tregs) in the blood and within the tumor microenvironment of GBM patients are known to contribute to their dismal immune responses. Here, we determined which chemokine secreted by gliomas can preferentially induce Treg recruitment and migration. In the malignant human glioma cell lines D-54, U-87, U-251, and LN-229, the chemokines CCL22 and CCL2 were detected by intracellular cytokine analysis. Furthermore, tumor cells from eight patients with GBM had a similar chemokine expression profile. However, only CCL2 was detected by enzyme-linked immunosorbent assay, indicating that CCL2 may be the principal chemokine for Treg migration in GBM patients. Interestingly, the Tregs from GBM patients had significantly higher expression levels of the CCL2 receptor CCR4 than did Tregs from healthy controls. Glioma supernatants and the recombinant human chemokines CCL2 and CCL22 induced Treg migration and were blocked by antibodies to the chemokine receptors. Production of CCL2 by glioma cells could also be mitigated by the chemotherapeutic agents temozolomide and carmustine [3-bis (2-chloroethyl)-1-nitrosourea]. Our results indicate that gliomas augment immunosuppression by selective chemokine-mediated recruitment of Tregs into the tumor microenvironment and that modulating this interaction with chemotherapy could facilitate the development of novel immunotherapeutics to malignant gliomas. |
| doi_str_mv | 10.1007/s00262-007-0336-x |
| format | Article |
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Farzana ; DeAngulo, Guillermo ; Prabhu, Sujit S. ; Heimberger, Amy B.</creator><creatorcontrib>Jordan, Justin T. ; Sun, Wei ; Hussain, S. Farzana ; DeAngulo, Guillermo ; Prabhu, Sujit S. ; Heimberger, Amy B.</creatorcontrib><description>Despite the immunogenicity of glioblastoma multiforme (GBM), immune-mediated eradication of these tumors remains deficient. Regulatory T cells (Tregs) in the blood and within the tumor microenvironment of GBM patients are known to contribute to their dismal immune responses. Here, we determined which chemokine secreted by gliomas can preferentially induce Treg recruitment and migration. In the malignant human glioma cell lines D-54, U-87, U-251, and LN-229, the chemokines CCL22 and CCL2 were detected by intracellular cytokine analysis. Furthermore, tumor cells from eight patients with GBM had a similar chemokine expression profile. However, only CCL2 was detected by enzyme-linked immunosorbent assay, indicating that CCL2 may be the principal chemokine for Treg migration in GBM patients. Interestingly, the Tregs from GBM patients had significantly higher expression levels of the CCL2 receptor CCR4 than did Tregs from healthy controls. Glioma supernatants and the recombinant human chemokines CCL2 and CCL22 induced Treg migration and were blocked by antibodies to the chemokine receptors. Production of CCL2 by glioma cells could also be mitigated by the chemotherapeutic agents temozolomide and carmustine [3-bis (2-chloroethyl)-1-nitrosourea]. Our results indicate that gliomas augment immunosuppression by selective chemokine-mediated recruitment of Tregs into the tumor microenvironment and that modulating this interaction with chemotherapy could facilitate the development of novel immunotherapeutics to malignant gliomas.</description><identifier>ISSN: 0340-7004</identifier><identifier>EISSN: 1432-0851</identifier><identifier>DOI: 10.1007/s00262-007-0336-x</identifier><identifier>PMID: 17522861</identifier><identifier>CODEN: CIIMDN</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer-Verlag</publisher><subject>Antineoplastic agents ; Antineoplastic Agents - pharmacology ; Biological and medical sciences ; Brain cancer ; Brain Neoplasms - drug therapy ; Brain Neoplasms - immunology ; Cancer Research ; Carmustine - pharmacology ; Cell Line, Tumor ; Cells ; Chemokine CCL2 - drug effects ; Chemokine CCL2 - metabolism ; Chemokine CCL22 - drug effects ; Chemokine CCL22 - metabolism ; Chemokines ; Chemokines - biosynthesis ; Chemokines - drug effects ; Chemotaxis, Leukocyte - drug effects ; Chemotherapy ; Cytoplasm - chemistry ; Dacarbazine - analogs & derivatives ; Dacarbazine - pharmacology ; Enzyme-Linked Immunosorbent Assay ; Enzymes ; Flow Cytometry ; Glioma - drug therapy ; Glioma - immunology ; Humans ; Immunology ; Immunotherapy ; Lymphocytes ; Medical sciences ; Medicine ; Medicine & Public Health ; Neurology ; Oncology ; Original ; Original Article ; Pharmacology. Drug treatments ; Receptors, CCR2 - biosynthesis ; Receptors, CCR4 - biosynthesis ; Scandals ; T-Lymphocytes, Regulatory - immunology ; T-Lymphocytes, Regulatory - metabolism ; Temozolomide ; Tumors ; Tumors of the nervous system. Phacomatoses</subject><ispartof>Cancer Immunology, Immunotherapy, 2008-01, Vol.57 (1), p.123-131</ispartof><rights>Springer-Verlag 2007</rights><rights>2008 INIST-CNRS</rights><rights>Springer-Verlag 2008</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c455t-455ed7aa9178a78a9ebfefefdd8072ae4dd21468817c0cd29656d1909583c0d93</citedby><cites>FETCH-LOGICAL-c455t-455ed7aa9178a78a9ebfefefdd8072ae4dd21468817c0cd29656d1909583c0d93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11030978/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11030978/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27922,27923,41486,42555,51317,53789,53791</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20145627$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17522861$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jordan, Justin T.</creatorcontrib><creatorcontrib>Sun, Wei</creatorcontrib><creatorcontrib>Hussain, S. Farzana</creatorcontrib><creatorcontrib>DeAngulo, Guillermo</creatorcontrib><creatorcontrib>Prabhu, Sujit S.</creatorcontrib><creatorcontrib>Heimberger, Amy B.</creatorcontrib><title>Preferential migration of regulatory T cells mediated by glioma-secreted chemokines can be blocked with chemotherapy</title><title>Cancer Immunology, Immunotherapy</title><addtitle>Cancer Immunol Immunother</addtitle><addtitle>Cancer Immunol Immunother</addtitle><description>Despite the immunogenicity of glioblastoma multiforme (GBM), immune-mediated eradication of these tumors remains deficient. Regulatory T cells (Tregs) in the blood and within the tumor microenvironment of GBM patients are known to contribute to their dismal immune responses. Here, we determined which chemokine secreted by gliomas can preferentially induce Treg recruitment and migration. In the malignant human glioma cell lines D-54, U-87, U-251, and LN-229, the chemokines CCL22 and CCL2 were detected by intracellular cytokine analysis. Furthermore, tumor cells from eight patients with GBM had a similar chemokine expression profile. However, only CCL2 was detected by enzyme-linked immunosorbent assay, indicating that CCL2 may be the principal chemokine for Treg migration in GBM patients. Interestingly, the Tregs from GBM patients had significantly higher expression levels of the CCL2 receptor CCR4 than did Tregs from healthy controls. Glioma supernatants and the recombinant human chemokines CCL2 and CCL22 induced Treg migration and were blocked by antibodies to the chemokine receptors. Production of CCL2 by glioma cells could also be mitigated by the chemotherapeutic agents temozolomide and carmustine [3-bis (2-chloroethyl)-1-nitrosourea]. Our results indicate that gliomas augment immunosuppression by selective chemokine-mediated recruitment of Tregs into the tumor microenvironment and that modulating this interaction with chemotherapy could facilitate the development of novel immunotherapeutics to malignant gliomas.</description><subject>Antineoplastic agents</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Brain cancer</subject><subject>Brain Neoplasms - drug therapy</subject><subject>Brain Neoplasms - immunology</subject><subject>Cancer Research</subject><subject>Carmustine - pharmacology</subject><subject>Cell Line, Tumor</subject><subject>Cells</subject><subject>Chemokine CCL2 - drug effects</subject><subject>Chemokine CCL2 - metabolism</subject><subject>Chemokine CCL22 - drug effects</subject><subject>Chemokine CCL22 - metabolism</subject><subject>Chemokines</subject><subject>Chemokines - biosynthesis</subject><subject>Chemokines - drug effects</subject><subject>Chemotaxis, Leukocyte - drug effects</subject><subject>Chemotherapy</subject><subject>Cytoplasm - chemistry</subject><subject>Dacarbazine - analogs & derivatives</subject><subject>Dacarbazine - pharmacology</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Enzymes</subject><subject>Flow Cytometry</subject><subject>Glioma - drug therapy</subject><subject>Glioma - immunology</subject><subject>Humans</subject><subject>Immunology</subject><subject>Immunotherapy</subject><subject>Lymphocytes</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Neurology</subject><subject>Oncology</subject><subject>Original</subject><subject>Original Article</subject><subject>Pharmacology. Drug treatments</subject><subject>Receptors, CCR2 - biosynthesis</subject><subject>Receptors, CCR4 - biosynthesis</subject><subject>Scandals</subject><subject>T-Lymphocytes, Regulatory - immunology</subject><subject>T-Lymphocytes, Regulatory - metabolism</subject><subject>Temozolomide</subject><subject>Tumors</subject><subject>Tumors of the nervous system. Phacomatoses</subject><issn>0340-7004</issn><issn>1432-0851</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp1UcFu1DAQtRCIbgsfwAVZSBwDYzuJnRNCFVCkSnAoZ8uxJ1m3TrzYWej-PV5l1cIByRqP5r2ZefYj5BWDdwxAvs8AvOVVSSsQoq3un5ANq0WpqIY9JRsQNVQSoD4j5znfloRD1z0nZ0w2nKuWbcjyPeGACefFm0AnPyaz-DjTONCE4z6YJaYDvaEWQ8h0QufNgo72BzoGHydTZbQJjyW7xSne-RkztWamPdI-RHtXkN9-2a7wssVkdocX5NlgQsaXp_uC_Pj86ebyqrr-9uXr5cfrytZNs1QloJPGdEwqU06H_VDEDs4pkNxg7RxndasUkxas413btI510DVKWHCduCAf1rm7fV-k2_LKZILeJT-ZdNDReP0vMvutHuMvzRgI6KQqE96cJqT4c4950bdxn-YiWnMmGgZKsEJiK8mmmHP5z4cNDPTRKL0apY_p0Sh9X3pe_y3tsePkTCG8PRFMtiYMyczW5wceB1Y3LZeFx1deLtA8YnpU-P_tfwBFfa6P</recordid><startdate>20080101</startdate><enddate>20080101</enddate><creator>Jordan, Justin T.</creator><creator>Sun, Wei</creator><creator>Hussain, S. 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Farzana ; DeAngulo, Guillermo ; Prabhu, Sujit S. ; Heimberger, Amy B.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c455t-455ed7aa9178a78a9ebfefefdd8072ae4dd21468817c0cd29656d1909583c0d93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Antineoplastic agents</topic><topic>Antineoplastic Agents - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Brain cancer</topic><topic>Brain Neoplasms - drug therapy</topic><topic>Brain Neoplasms - immunology</topic><topic>Cancer Research</topic><topic>Carmustine - pharmacology</topic><topic>Cell Line, Tumor</topic><topic>Cells</topic><topic>Chemokine CCL2 - drug effects</topic><topic>Chemokine CCL2 - metabolism</topic><topic>Chemokine CCL22 - drug effects</topic><topic>Chemokine CCL22 - metabolism</topic><topic>Chemokines</topic><topic>Chemokines - biosynthesis</topic><topic>Chemokines - drug effects</topic><topic>Chemotaxis, Leukocyte - drug effects</topic><topic>Chemotherapy</topic><topic>Cytoplasm - chemistry</topic><topic>Dacarbazine - analogs & derivatives</topic><topic>Dacarbazine - pharmacology</topic><topic>Enzyme-Linked Immunosorbent Assay</topic><topic>Enzymes</topic><topic>Flow Cytometry</topic><topic>Glioma - drug therapy</topic><topic>Glioma - immunology</topic><topic>Humans</topic><topic>Immunology</topic><topic>Immunotherapy</topic><topic>Lymphocytes</topic><topic>Medical sciences</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Neurology</topic><topic>Oncology</topic><topic>Original</topic><topic>Original Article</topic><topic>Pharmacology. Drug treatments</topic><topic>Receptors, CCR2 - biosynthesis</topic><topic>Receptors, CCR4 - biosynthesis</topic><topic>Scandals</topic><topic>T-Lymphocytes, Regulatory - immunology</topic><topic>T-Lymphocytes, Regulatory - metabolism</topic><topic>Temozolomide</topic><topic>Tumors</topic><topic>Tumors of the nervous system. Phacomatoses</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jordan, Justin T.</creatorcontrib><creatorcontrib>Sun, Wei</creatorcontrib><creatorcontrib>Hussain, S. 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Farzana</au><au>DeAngulo, Guillermo</au><au>Prabhu, Sujit S.</au><au>Heimberger, Amy B.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Preferential migration of regulatory T cells mediated by glioma-secreted chemokines can be blocked with chemotherapy</atitle><jtitle>Cancer Immunology, Immunotherapy</jtitle><stitle>Cancer Immunol Immunother</stitle><addtitle>Cancer Immunol Immunother</addtitle><date>2008-01-01</date><risdate>2008</risdate><volume>57</volume><issue>1</issue><spage>123</spage><epage>131</epage><pages>123-131</pages><issn>0340-7004</issn><eissn>1432-0851</eissn><coden>CIIMDN</coden><abstract>Despite the immunogenicity of glioblastoma multiforme (GBM), immune-mediated eradication of these tumors remains deficient. Regulatory T cells (Tregs) in the blood and within the tumor microenvironment of GBM patients are known to contribute to their dismal immune responses. Here, we determined which chemokine secreted by gliomas can preferentially induce Treg recruitment and migration. In the malignant human glioma cell lines D-54, U-87, U-251, and LN-229, the chemokines CCL22 and CCL2 were detected by intracellular cytokine analysis. Furthermore, tumor cells from eight patients with GBM had a similar chemokine expression profile. However, only CCL2 was detected by enzyme-linked immunosorbent assay, indicating that CCL2 may be the principal chemokine for Treg migration in GBM patients. Interestingly, the Tregs from GBM patients had significantly higher expression levels of the CCL2 receptor CCR4 than did Tregs from healthy controls. Glioma supernatants and the recombinant human chemokines CCL2 and CCL22 induced Treg migration and were blocked by antibodies to the chemokine receptors. Production of CCL2 by glioma cells could also be mitigated by the chemotherapeutic agents temozolomide and carmustine [3-bis (2-chloroethyl)-1-nitrosourea]. Our results indicate that gliomas augment immunosuppression by selective chemokine-mediated recruitment of Tregs into the tumor microenvironment and that modulating this interaction with chemotherapy could facilitate the development of novel immunotherapeutics to malignant gliomas.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer-Verlag</pub><pmid>17522861</pmid><doi>10.1007/s00262-007-0336-x</doi><tpages>9</tpages></addata></record> |
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| subjects | Antineoplastic agents Antineoplastic Agents - pharmacology Biological and medical sciences Brain cancer Brain Neoplasms - drug therapy Brain Neoplasms - immunology Cancer Research Carmustine - pharmacology Cell Line, Tumor Cells Chemokine CCL2 - drug effects Chemokine CCL2 - metabolism Chemokine CCL22 - drug effects Chemokine CCL22 - metabolism Chemokines Chemokines - biosynthesis Chemokines - drug effects Chemotaxis, Leukocyte - drug effects Chemotherapy Cytoplasm - chemistry Dacarbazine - analogs & derivatives Dacarbazine - pharmacology Enzyme-Linked Immunosorbent Assay Enzymes Flow Cytometry Glioma - drug therapy Glioma - immunology Humans Immunology Immunotherapy Lymphocytes Medical sciences Medicine Medicine & Public Health Neurology Oncology Original Original Article Pharmacology. Drug treatments Receptors, CCR2 - biosynthesis Receptors, CCR4 - biosynthesis Scandals T-Lymphocytes, Regulatory - immunology T-Lymphocytes, Regulatory - metabolism Temozolomide Tumors Tumors of the nervous system. Phacomatoses |
| title | Preferential migration of regulatory T cells mediated by glioma-secreted chemokines can be blocked with chemotherapy |
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