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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
13
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pubmed:dateCreated |
2002-7-4
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pubmed:abstractText |
Interleukin (IL) 12 treatment in the CSA1M and OV-HM, but not in Meth A tumor models,induces tumor regression that is associated with T-cell migration to tumor sites.Here, we investigated the role of the CC chemokine receptor (CCR)5 in T-cell migration induced after IL-12 treatment. In the two IL-12-responsive tumor models (CSA1M and OV-HM), IL-12 treatment up-regulated the mRNA expression of CCR5 in splenic T cells as well as ligands for CCR5, such as macrophage inflammatory protein (MIP) 1alpha and MIP-1beta in tumor masses. In contrast, the expression of CCR5 in spleens and MIP-1alpha/MIP-1beta in tumor masses was marginally induced before and even after IL-12 treatment in the Meth A model in which T-cell migration is not observed. T cells infiltrating tumor masses in the former two IL-12-responsive models expressed CCR5. Administration of a synthetic CCR5 antagonist TAK-779 to tumor-bearing mice during IL-12 immunotherapy prevented T-cell migration and tumor regression. Furthermore, anti-CCR5 antibody was found to inhibit T-cell migration in the lymphoid cell migration assay. Namely, although splenic T cells prepared from IL-12-treated CSA1M or OV-HM-bearing mice migrated into the corresponding tumor masses in recipient mice, the migration was inhibited when donor T cells were treated with anti-CCR5 antibody before the injection. These results indicate a critical role for CCR5 in the induction of T-cell migration to tumor sites after IL-12 treatment.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Amides,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CCL3,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CCL4,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-12,
http://linkedlifedata.com/resource/pubmed/chemical/Macrophage Inflammatory Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Quaternary Ammonium Compounds,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, CCR5,
http://linkedlifedata.com/resource/pubmed/chemical/TAK 779
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0008-5472
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pubmed:author |
pubmed-author:FujiwaraHiromiH,
pubmed-author:GaoPingP,
pubmed-author:HamaokaToshiyukiT,
pubmed-author:HigashibataYujiY,
pubmed-author:ImanishiTakeshiT,
pubmed-author:KitamuraYukihikoY,
pubmed-author:MatsushimaKoujiK,
pubmed-author:MukaiTakaoT,
pubmed-author:MuraiMasakoM,
pubmed-author:NomuraShintaroS,
pubmed-author:ObikaSatoshiS,
pubmed-author:UekusaYasuhiroY,
pubmed-author:YamaguchiNobuyaN,
pubmed-author:YuWen-GongWG
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pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
62
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
3751-8
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:12097285-Amides,
pubmed-meshheading:12097285-Animals,
pubmed-meshheading:12097285-Cell Movement,
pubmed-meshheading:12097285-Chemokine CCL3,
pubmed-meshheading:12097285-Chemokine CCL4,
pubmed-meshheading:12097285-Female,
pubmed-meshheading:12097285-Fibrosarcoma,
pubmed-meshheading:12097285-Humans,
pubmed-meshheading:12097285-Interleukin-12,
pubmed-meshheading:12097285-Lymphocytes, Tumor-Infiltrating,
pubmed-meshheading:12097285-Macrophage Inflammatory Proteins,
pubmed-meshheading:12097285-Male,
pubmed-meshheading:12097285-Mice,
pubmed-meshheading:12097285-Mice, Inbred BALB C,
pubmed-meshheading:12097285-Mice, Inbred C3H,
pubmed-meshheading:12097285-Mice, Inbred C57BL,
pubmed-meshheading:12097285-Neoplasms, Experimental,
pubmed-meshheading:12097285-Quaternary Ammonium Compounds,
pubmed-meshheading:12097285-RNA, Messenger,
pubmed-meshheading:12097285-Receptors, CCR5,
pubmed-meshheading:12097285-Spleen,
pubmed-meshheading:12097285-T-Lymphocytes,
pubmed-meshheading:12097285-Up-Regulation
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pubmed:year |
2002
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pubmed:articleTitle |
A pivotal role for CC chemokine receptor 5 in T-cell migration to tumor sites induced by interleukin 12 treatment in tumor-bearing mice.
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pubmed:affiliation |
Department of Oncology, Biomedical Research Center, Osaka University Graduate School of Medicine, Suita, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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