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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
2
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pubmed:dateCreated |
2011-2-11
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pubmed:abstractText |
Successful immune-mediated regression of solid tumors is difficult because of the small number of cytotoxic T lymphocytes (CTLs) that were traffic to the tumor site. Here, the targeting of tumor-specific infiltrating CTLs was dependent on a fusion protein consisting of human epidermal growth factor (EGF) and staphylococcal enterotoxin A (SEA) with the D227A mutation. EGF-SEA strongly restrained the growth of murine solid sarcoma 180 (S180) tumors (control versus EGF-SEA, mean tumor weight: 1.013 versus 0.197 g, difference ?=?0.816 g). In mice treated with EGF-SEA, CD4+, CD8+ and SEA-reactive T lymphocytes were enriched around the EGFR expressing tumor cells. The EGF receptors were potentially phosphorylated by EGF-SEA stimulation and the fusion protein promoted T cells to release the tumoricidal cytokines interferon-? (IFN-?) and tumor necrosis factor-? (TNF-?). Intratumoral CTLs secreted cytolytic pore-forming perforins and granzyme B proteins near the surface of carcinomas, causing the death of many tumor cells. We additionally show that labeled EGF-SEA was directly targeted to the tumor tissue after intravenous (i.v.) injection. The findings demonstrate that antibody-like EGF-SEA plays an important role in arresting CTLs in the solid tumor site and has therapeutic potential as a tumor-targeting agent.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/21311755-10706880,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21311755-10878347,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21311755-10918198,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21311755-11251975,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21311755-11410615,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21311755-11467954,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21311755-11922388,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21311755-12297282,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21311755-12766484,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21311755-1399401,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21311755-14593228,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21311755-15671563,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21311755-16041532,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21311755-16125469,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21311755-17116735,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21311755-17310380,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21311755-19254476,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21311755-1939154,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21311755-2311877,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21311755-2785644,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21311755-3488814,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21311755-3584106,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21311755-6304537,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21311755-6602382,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21311755-7568219,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21311755-7734048,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21311755-7734049,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21311755-7876195,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21311755-8090750,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21311755-8156501,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21311755-9058731,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21311755-9122222,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21311755-9195941,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21311755-9605129,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21311755-9661898,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21311755-9930679
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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 |
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pubmed:status |
MEDLINE
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pubmed:issn |
1932-6203
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:volume |
6
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
e16642
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pubmed:meshHeading |
pubmed-meshheading:21311755-Amino Acid Substitution,
pubmed-meshheading:21311755-Animals,
pubmed-meshheading:21311755-Cells, Cultured,
pubmed-meshheading:21311755-Chemotaxis, Leukocyte,
pubmed-meshheading:21311755-Cytotoxicity, Immunologic,
pubmed-meshheading:21311755-Enterotoxins,
pubmed-meshheading:21311755-Humans,
pubmed-meshheading:21311755-Immunotherapy, Adoptive,
pubmed-meshheading:21311755-Lymphocytes, Tumor-Infiltrating,
pubmed-meshheading:21311755-Male,
pubmed-meshheading:21311755-Mice,
pubmed-meshheading:21311755-Mice, Inbred ICR,
pubmed-meshheading:21311755-Mutation, Missense,
pubmed-meshheading:21311755-Recombinant Fusion Proteins,
pubmed-meshheading:21311755-Superantigens,
pubmed-meshheading:21311755-T-Lymphocytes, Cytotoxic,
pubmed-meshheading:21311755-Tumor Necrosis Factor-alpha
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pubmed:year |
2011
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pubmed:articleTitle |
Solid tumor-targeted infiltrating cytotoxic T lymphocytes retained by a superantigen fusion protein.
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pubmed:affiliation |
Key Laboratory of Industrial Microbiology, Ministry of Education, College of Biotechnology, Tianjin University of Science and Technology, Tianjin, People's Republic of China. jialinsun@tust.edu.cn
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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