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Characterization of the CCL21-mediated melanoma-specific immune responses and in situ melanoma eradication
Previous studies have shown that secondary lymphoid chemokine, CCL21, can be used for modulation of tumor-specific immune responses. Here, using B16F0 melanoma cells stably expressing CCL21 under the control of cytomegalovirus and ubiquitin promoters, we showed that CCL21-activated immune responses...
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| Published in: | Molecular cancer therapeutics 2007-06, Vol.6 (6), p.1755-1764 |
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| cites | cdi_FETCH-LOGICAL-c417t-21df5439403b72ea924ce79ca7b4a03af1bf00d4ee4871240c8bac9a0a16da273 |
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| container_title | Molecular cancer therapeutics |
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| creator | Novak, Laura Igoucheva, Olga Cho, Stephanie Alexeev, Vitali |
| description | Previous studies have shown that secondary lymphoid chemokine, CCL21, can be used for modulation of tumor-specific immune
responses. Here, using B16F0 melanoma cells stably expressing CCL21 under the control of cytomegalovirus and ubiquitin promoters,
we showed that CCL21-activated immune responses depend on the amount of melanoma-derived chemokine, which, in turn, depends
on the strength of the promoter. We showed that ubiquitin promoter–driven expression of CCL21 enabled massive infiltration
of tumors with CD4 + CD25 − , CD8 + T lymphocytes, and CD11c + dendritic cells, and consequent activation of cellular and humoral immune responses sufficient for complete rejection of
CCL21-positive melanomas within 3 weeks in all tumor-inoculated mice. Mice that rejected CCL21-positive tumors acquired protective
immunity against melanoma, which was transferable to naive mice via splenocytes and central memory T cells. Moreover, melanoma-derived
CCL21 facilitated immune-mediated remission of preestablished, distant wild-type melanomas. Overall, these results suggest
that elevated levels of tumor-derived CCL21 are required for the activation of strong melanoma-specific immune responses and
generation of protective immunologic memory. They also open new perspectives for the development of novel vaccination strategies
against melanoma, which use intratumoral delivery of the optimized CCL21-encoding vectors in conjunction with DNA-based vaccines.
[Mol Cancer Ther 2007;6(6):1–10] |
| doi_str_mv | 10.1158/1535-7163.MCT-06-0709 |
| format | article |
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responses. Here, using B16F0 melanoma cells stably expressing CCL21 under the control of cytomegalovirus and ubiquitin promoters,
we showed that CCL21-activated immune responses depend on the amount of melanoma-derived chemokine, which, in turn, depends
on the strength of the promoter. We showed that ubiquitin promoter–driven expression of CCL21 enabled massive infiltration
of tumors with CD4 + CD25 − , CD8 + T lymphocytes, and CD11c + dendritic cells, and consequent activation of cellular and humoral immune responses sufficient for complete rejection of
CCL21-positive melanomas within 3 weeks in all tumor-inoculated mice. Mice that rejected CCL21-positive tumors acquired protective
immunity against melanoma, which was transferable to naive mice via splenocytes and central memory T cells. Moreover, melanoma-derived
CCL21 facilitated immune-mediated remission of preestablished, distant wild-type melanomas. Overall, these results suggest
that elevated levels of tumor-derived CCL21 are required for the activation of strong melanoma-specific immune responses and
generation of protective immunologic memory. They also open new perspectives for the development of novel vaccination strategies
against melanoma, which use intratumoral delivery of the optimized CCL21-encoding vectors in conjunction with DNA-based vaccines.
[Mol Cancer Ther 2007;6(6):1–10]</description><identifier>ISSN: 1535-7163</identifier><identifier>EISSN: 1538-8514</identifier><identifier>DOI: 10.1158/1535-7163.MCT-06-0709</identifier><identifier>PMID: 17575105</identifier><language>eng</language><publisher>United States: American Association for Cancer Research</publisher><subject>Animals ; Antibody Formation ; Base Sequence ; Chemokine CCL21 ; Chemokines, CC - physiology ; Cytomegalovirus ; DNA Primers ; immune response ; Immunity, Cellular ; immunotherapy ; melanoma ; Melanoma, Experimental - immunology ; Mice ; secondary lymphoid chemokine</subject><ispartof>Molecular cancer therapeutics, 2007-06, Vol.6 (6), p.1755-1764</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c417t-21df5439403b72ea924ce79ca7b4a03af1bf00d4ee4871240c8bac9a0a16da273</citedby><cites>FETCH-LOGICAL-c417t-21df5439403b72ea924ce79ca7b4a03af1bf00d4ee4871240c8bac9a0a16da273</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17575105$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Novak, Laura</creatorcontrib><creatorcontrib>Igoucheva, Olga</creatorcontrib><creatorcontrib>Cho, Stephanie</creatorcontrib><creatorcontrib>Alexeev, Vitali</creatorcontrib><title>Characterization of the CCL21-mediated melanoma-specific immune responses and in situ melanoma eradication</title><title>Molecular cancer therapeutics</title><addtitle>Mol Cancer Ther</addtitle><description>Previous studies have shown that secondary lymphoid chemokine, CCL21, can be used for modulation of tumor-specific immune
responses. Here, using B16F0 melanoma cells stably expressing CCL21 under the control of cytomegalovirus and ubiquitin promoters,
we showed that CCL21-activated immune responses depend on the amount of melanoma-derived chemokine, which, in turn, depends
on the strength of the promoter. We showed that ubiquitin promoter–driven expression of CCL21 enabled massive infiltration
of tumors with CD4 + CD25 − , CD8 + T lymphocytes, and CD11c + dendritic cells, and consequent activation of cellular and humoral immune responses sufficient for complete rejection of
CCL21-positive melanomas within 3 weeks in all tumor-inoculated mice. Mice that rejected CCL21-positive tumors acquired protective
immunity against melanoma, which was transferable to naive mice via splenocytes and central memory T cells. Moreover, melanoma-derived
CCL21 facilitated immune-mediated remission of preestablished, distant wild-type melanomas. Overall, these results suggest
that elevated levels of tumor-derived CCL21 are required for the activation of strong melanoma-specific immune responses and
generation of protective immunologic memory. They also open new perspectives for the development of novel vaccination strategies
against melanoma, which use intratumoral delivery of the optimized CCL21-encoding vectors in conjunction with DNA-based vaccines.
[Mol Cancer Ther 2007;6(6):1–10]</description><subject>Animals</subject><subject>Antibody Formation</subject><subject>Base Sequence</subject><subject>Chemokine CCL21</subject><subject>Chemokines, CC - physiology</subject><subject>Cytomegalovirus</subject><subject>DNA Primers</subject><subject>immune response</subject><subject>Immunity, Cellular</subject><subject>immunotherapy</subject><subject>melanoma</subject><subject>Melanoma, Experimental - immunology</subject><subject>Mice</subject><subject>secondary lymphoid chemokine</subject><issn>1535-7163</issn><issn>1538-8514</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><recordid>eNqFkcFO3DAQhq2qVaHAIxT5VE4Gj2PHyRFFLa20FRd6tibOpDHaJIudqCpPj5dd0WPlw1ijb8bW9zP2GeQ1gKluwBRGWCiL65_Ng5ClkFbW79hp7leiMqDfv94PzAn7lNKjlFDVCj6yE7DGGpDmlD02A0b0C8XwjEuYJz73fBmIN81GgRipC7hQx0fa4jSPKNKOfOiD52Ec14l4pLSbp0SJ49TxMPEUlvUN5xSxC_518zn70OM20cWxnrFf374-NN_F5v7uR3O7EV6DXYSCrje6qLUsWqsIa6U92dqjbTXKAntoeyk7TaQrC0pLX7Xoa5QIZYfKFmfsy2HvLs5PK6XFjSF52uYf0bwmZ2UJCkrzX1DJqqjLGjJoDqCPc0qRereLYcT414F0-zTc3rTbm3Y5DSdLt08jz10eH1jbbPLf1FF_Bq4OwBB-D39CJOdx8hSzVMLoB1fmk2lTvAB2n5SY</recordid><startdate>20070601</startdate><enddate>20070601</enddate><creator>Novak, Laura</creator><creator>Igoucheva, Olga</creator><creator>Cho, Stephanie</creator><creator>Alexeev, Vitali</creator><general>American Association for Cancer Research</general><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>7U9</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>20070601</creationdate><title>Characterization of the CCL21-mediated melanoma-specific immune responses and in situ melanoma eradication</title><author>Novak, Laura ; Igoucheva, Olga ; Cho, Stephanie ; Alexeev, Vitali</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c417t-21df5439403b72ea924ce79ca7b4a03af1bf00d4ee4871240c8bac9a0a16da273</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Animals</topic><topic>Antibody Formation</topic><topic>Base Sequence</topic><topic>Chemokine CCL21</topic><topic>Chemokines, CC - physiology</topic><topic>Cytomegalovirus</topic><topic>DNA Primers</topic><topic>immune response</topic><topic>Immunity, Cellular</topic><topic>immunotherapy</topic><topic>melanoma</topic><topic>Melanoma, Experimental - immunology</topic><topic>Mice</topic><topic>secondary lymphoid chemokine</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Novak, Laura</creatorcontrib><creatorcontrib>Igoucheva, Olga</creatorcontrib><creatorcontrib>Cho, Stephanie</creatorcontrib><creatorcontrib>Alexeev, Vitali</creatorcontrib><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>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Molecular cancer therapeutics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Novak, Laura</au><au>Igoucheva, Olga</au><au>Cho, Stephanie</au><au>Alexeev, Vitali</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Characterization of the CCL21-mediated melanoma-specific immune responses and in situ melanoma eradication</atitle><jtitle>Molecular cancer therapeutics</jtitle><addtitle>Mol Cancer Ther</addtitle><date>2007-06-01</date><risdate>2007</risdate><volume>6</volume><issue>6</issue><spage>1755</spage><epage>1764</epage><pages>1755-1764</pages><issn>1535-7163</issn><eissn>1538-8514</eissn><abstract>Previous studies have shown that secondary lymphoid chemokine, CCL21, can be used for modulation of tumor-specific immune
responses. Here, using B16F0 melanoma cells stably expressing CCL21 under the control of cytomegalovirus and ubiquitin promoters,
we showed that CCL21-activated immune responses depend on the amount of melanoma-derived chemokine, which, in turn, depends
on the strength of the promoter. We showed that ubiquitin promoter–driven expression of CCL21 enabled massive infiltration
of tumors with CD4 + CD25 − , CD8 + T lymphocytes, and CD11c + dendritic cells, and consequent activation of cellular and humoral immune responses sufficient for complete rejection of
CCL21-positive melanomas within 3 weeks in all tumor-inoculated mice. Mice that rejected CCL21-positive tumors acquired protective
immunity against melanoma, which was transferable to naive mice via splenocytes and central memory T cells. Moreover, melanoma-derived
CCL21 facilitated immune-mediated remission of preestablished, distant wild-type melanomas. Overall, these results suggest
that elevated levels of tumor-derived CCL21 are required for the activation of strong melanoma-specific immune responses and
generation of protective immunologic memory. They also open new perspectives for the development of novel vaccination strategies
against melanoma, which use intratumoral delivery of the optimized CCL21-encoding vectors in conjunction with DNA-based vaccines.
[Mol Cancer Ther 2007;6(6):1–10]</abstract><cop>United States</cop><pub>American Association for Cancer Research</pub><pmid>17575105</pmid><doi>10.1158/1535-7163.MCT-06-0709</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Molecular cancer therapeutics, 2007-06, Vol.6 (6), p.1755-1764 |
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| language | eng |
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| source | EZB Electronic Journals Library |
| subjects | Animals Antibody Formation Base Sequence Chemokine CCL21 Chemokines, CC - physiology Cytomegalovirus DNA Primers immune response Immunity, Cellular immunotherapy melanoma Melanoma, Experimental - immunology Mice secondary lymphoid chemokine |
| title | Characterization of the CCL21-mediated melanoma-specific immune responses and in situ melanoma eradication |
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