CXCL11型
CXCL10型
CXCR3型
CXCL9型
血管生成
细胞毒性T细胞
癌症研究
CCL17型
CD8型
体内
趋化因子
CCL5
CXCL14型
免疫学
化学
生物
趋化因子受体
体外
抗原
免疫系统
白细胞介素2受体
生物化学
生物技术
作者
Paul J. Hensbergen,Pepijn G.J.T.B. Wijnands,Marco W. J. Schreurs,Rik J. Scheper,Rein Willemze,Cornelis P. Tensen
出处
期刊:Journal of Immunotherapy
[Ovid Technologies (Wolters Kluwer)]
日期:2005-07-01
卷期号:28 (4): 343-351
被引量:117
标识
DOI:10.1097/01.cji.0000165355.26795.27
摘要
The IFN-gamma-inducible and CXCR3-targeting human CXC chemokines CXCL9 (Mig) and CXCL10 (IP10) have potent antitumor activity through attraction of cytotoxic T lymphocytes and inhibition of angiogenesis. The more recently identified CXCR3-targeting chemokine CXCL11 (I-TAC/IP9) proved to be a more potent chemokine than CXCL9 and CXCL10 in vitro, both in chemotaxis assays with CXCR3+ T lymphocytes and in calcium mobilization experiments. However, its antitumor activity in vivo has not been shown so far. To investigate this, mice were challenged with EL4 T-cell lymphoma cells, genetically modified to produce murine CXCL11. Tumor growth curves showed complete rejection of CXCL11-producing tumors but not of control tumors. Tumor infiltrate analysis by flow cytometry showed a clear correlation between rejection of CXCL11-producing tumors and an increase of tumor-infiltrating CD8+CXCR3+ as well as CD8+CXCR3- T lymphocytes. In vivo CD8 T-cell depletion completely abrogated the antitumor effect. No difference in angiogenesis between control and CXCL11-producing tumors was observed. In survivors, rechallenge experiments with wild-type tumor cells suggested development of protective antitumor immunity involving tumor-specific IFN-gamma production by CD8+ T lymphocytes. These experiments show, for the first time, antitumor activity of CXCL11 in vivo, which warrants exploration for its potential role in anticancer immunotherapy.
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