| Title |
Human IP10-scFv and DC-induced CTL synergistically inhibit the growth of glioma in a xenograft model
|
|---|---|
| Published in |
Tumor Biology, May 2014
|
| DOI | 10.1007/s13277-014-1867-3 |
| Pubmed ID | |
| Authors |
Xuan Wang, Fang-Cheng Zhang, Hong-Yang Zhao, Xiao-Ling Lu, Yun Sun, Zhi-Yong Xiong, Xiao-Bing Jiang |
| Abstract |
The epidermal growth factor receptor (EGFR) mutant of EGFRvIII is highly expressed in glioma cells, and the EGFRvIII-specific dendritic cell (DC)-induced tumor antigen-specific CD8(+) cytotoxic T lymphocytes (CTLs) may hold promise in cancer immunotherapy. Interferon (IFN)-γ-inducible protein (IP)-10 (IP-10) is a potent inhibitor of angiogenesis and can recruit CXCR3(+) T cells, including CD8(+) T cells, which are important for the control of tumor growth. In this study, we assessed if the combination of IP10-EGFRvIIIscFv with DC-induced CTLs would improve the therapeutic antitumor efficacy. IP10-scFv was generated by linking the human IP-10 gene with the DNA fragment for anti-EGFRvIIIscFv with a (Gly4Ser)3 flexible linker, purified by affinity chromatography, and characterized for its anti-EGFRvIII immunoreactivity and chemotactic activity. DCs were isolated from human peripheral blood monocyte cells and pulsed with EGFRvIII-peptide, then co-cultured with autologous CD8(+) T cells. BALB/c-nu mice were inoculated with human glioma U87-EGFRvIII cells in the brain and treated intracranially with IP10-scFv and/or intravenously with DC-induced CTLs for evaluating the therapeutic effect. Treatment with both IP10-scFv and EGFRvIII peptide-pulsed, DC-induced CTL synergistically inhibited the growth of glioma and prolonged the survival of tumor-bearing mice, which was accompanied by the inhibition of tumor angiogenesis and enhancement of cytotoxicity, thereby increasing the numbers of brain-infiltrating lymphocytes (BILs) and prolonging the residence time of CTLs in the tumor. |
X Demographics
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Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 1 | 100% |
Demographic breakdown
| Type | Count | As % |
|---|---|---|
| Members of the public | 1 | 100% |
Mendeley readers
The data shown below were compiled from readership statistics for 19 Mendeley readers of this research output. Click here to see the associated Mendeley record.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 19 | 100% |
Demographic breakdown
| Readers by professional status | Count | As % |
|---|---|---|
| Researcher | 6 | 32% |
| Student > Bachelor | 3 | 16% |
| Student > Ph. D. Student | 3 | 16% |
| Student > Doctoral Student | 2 | 11% |
| Student > Master | 1 | 5% |
| Other | 2 | 11% |
| Unknown | 2 | 11% |
| Readers by discipline | Count | As % |
|---|---|---|
| Biochemistry, Genetics and Molecular Biology | 4 | 21% |
| Medicine and Dentistry | 4 | 21% |
| Agricultural and Biological Sciences | 3 | 16% |
| Immunology and Microbiology | 2 | 11% |
| Pharmacology, Toxicology and Pharmaceutical Science | 1 | 5% |
| Other | 3 | 16% |
| Unknown | 2 | 11% |
Attention Score in Context
This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 15 January 2015.
All research outputs
#19,015,492
of 23,577,654 outputs
Outputs from Tumor Biology
#1,388
of 2,634 outputs
Outputs of similar age
#165,859
of 228,726 outputs
Outputs of similar age from Tumor Biology
#52
of 88 outputs
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