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rdf:type |
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lifeskim:mentions |
umls-concept:C0033414,
umls-concept:C0035015,
umls-concept:C0038952,
umls-concept:C0039194,
umls-concept:C0085358,
umls-concept:C1332717,
umls-concept:C1413244,
umls-concept:C1449699,
umls-concept:C1516670,
umls-concept:C1548437,
umls-concept:C1706438,
umls-concept:C1831875,
umls-concept:C1882923,
umls-concept:C2349975,
umls-concept:C2698600
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pubmed:issue |
12
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pubmed:dateCreated |
2002-6-17
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pubmed:abstractText |
Anti-4-1BB monoclonal antibody (mAb) has been shown to induce antitumor immunity by a CD4/CD8-dependent mechanism, but its direct effect on tumor-specific CD8+ T cells in tumor rejection is unclear. Here we used transgenic CD8+ T cells against the unmutated tumor rejection antigen P1A to analyze whether this mAb can promote CD8+ T-cell function against large tumors in the absence of CD4+ T-helper cells. RAG-2(-/-) mice were challenged with P1A-expressing plasmacytoma J558. Once tumor size reached a diameter of 0.85-1.75 cm, mice were treated with P1A-specific CD8+ CTL (P1CTL) in conjunction with anti-4-1BB mAb or control IgG. All of the mice showed a partial regression of tumor, but mice treated with anti-4-1BB mAb exhibited markedly enhanced tumor rejection, delayed tumor progression, and prolonged survival. Correspondingly, we observed a substantial increase in the number of P1CTL in anti-4-1BB mAb-treated mice. Surprisingly, anti-4-1BB mAb did not accelerate division of the tumor-specific CD8+ T cells, and the increase in tumor-specific T-cell number was due to reduced activation-induced cell death. These results indicate that anti-4-1BB mAb can promote CD8+ T cell-mediated protection against large tumors in the absence of CD4+ T-cell help by promoting P1CTL survival without increasing initial clonal expansion.
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pubmed:grant |
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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/Antibodies, Monoclonal,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD137,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Neoplasm,
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Epitopes, T-Lymphocyte,
http://linkedlifedata.com/resource/pubmed/chemical/Rag2 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Nerve Growth Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Tumor Necrosis Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Tnfrsf9 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/V(D)J recombination activating...,
http://linkedlifedata.com/resource/pubmed/chemical/tumor rejection antigen P815A, mouse
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0008-5472
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
15
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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 |
3459-65
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:12067989-Animals,
pubmed-meshheading:12067989-Antibodies, Monoclonal,
pubmed-meshheading:12067989-Antigens, CD,
pubmed-meshheading:12067989-Antigens, CD137,
pubmed-meshheading:12067989-Antigens, Neoplasm,
pubmed-meshheading:12067989-CD8-Positive T-Lymphocytes,
pubmed-meshheading:12067989-Cell Death,
pubmed-meshheading:12067989-DNA-Binding Proteins,
pubmed-meshheading:12067989-Epitopes, T-Lymphocyte,
pubmed-meshheading:12067989-Immunotherapy, Adoptive,
pubmed-meshheading:12067989-Lymphocyte Activation,
pubmed-meshheading:12067989-Mice,
pubmed-meshheading:12067989-Mice, Inbred BALB C,
pubmed-meshheading:12067989-Mice, Transgenic,
pubmed-meshheading:12067989-Plasmacytoma,
pubmed-meshheading:12067989-Receptors, Nerve Growth Factor,
pubmed-meshheading:12067989-Receptors, Tumor Necrosis Factor,
pubmed-meshheading:12067989-T-Lymphocytes, Cytotoxic,
pubmed-meshheading:12067989-Tumor Cells, Cultured
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pubmed:year |
2002
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pubmed:articleTitle |
Anti-4-1BB monoclonal antibody enhances rejection of large tumor burden by promoting survival but not clonal expansion of tumor-specific CD8+ T cells.
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pubmed:affiliation |
Division of Cancer Immunology, Department of Pathology and Comprehensive Cancer Center, Ohio State University Medical Center, Columbus 43210, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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