Interleukin 7 induces CD4+ T cell-dependent tumor rejection.
Interleukin 7 induces CD4+ T cell-dependent tumor rejection.
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白介素7诱导CD4+ T细胞依赖性肿瘤排斥。
DOI：
10.1084/jem.174.6.1291
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发表时间：
1991-12-01
影响因子：
15.3
通讯作者：
BLANKENSTEIN, T
中科院分区：
文献类型：
--
作者：
HOCK, H;DORSCH, M;DIAMANTSTEIN, T;BLANKENSTEIN, T
分析了白介素7(IL-7)在体内诱导抗肿瘤反应的可能性。因此，IL-7基因在浆细胞瘤细胞系J558L中得到了表达。尽管产生IL-7的细胞在体外的生长没有受到抑制，但当注射到小鼠体内时，产生IL-7的细胞被完全排斥。仅在同基因小鼠中观察到肿瘤排斥反应，而在裸鼠中未观察到。平行注射抗IL-7单抗可消除其抑瘤作用。免疫组织化学分析显示，肿瘤组织中存在依赖IL-7的CD4+和CD8+T淋巴细胞，以及补体受体3型阳性(CR3+)细胞，主要是巨噬细胞。荷瘤小鼠T细胞亚群的耗尽表明抗肿瘤反应完全依赖于CD4+细胞，而肿瘤排斥反应不受CD8+细胞耗尽的影响。除CD4+细胞外，肿瘤排斥反应也需要CR3+细胞。IL-7基因在另一种不同细胞来源的肿瘤细胞系中的表达证实了IL-7的抗肿瘤作用。总之，我们的结果表明，通过肿瘤细胞靶向基因转移在肿瘤部位获得的高局部IL-7浓度会导致肿瘤排斥反应，其涉及的细胞机制似乎与其他细胞因子的类似实验中观察到的不同。
The potential of interleukin 7 (IL-7) to induce an antitumor response in vivo was analyzed. Therefore, the IL-7 gene was expressed in the plasmacytoma cell line J558L. Although the growth of IL-7-producing cells was not retarded in vitro, the IL-7-producing cells were completely rejected upon injection into mice. Tumor rejection was observed only in syngeneic but not in nude mice. The tumor-suppressive effect could be abolished by the parallel injection of an anti-IL-7 monoclonal antibody. Immunohistochemical analysis revealed IL-7- dependent infiltration of the tumor tissue by CD4+ and CD8+ T lymphocytes, and also type 3 complement receptor-positive (CR3+) cells, predominantly macrophages. Depletion of T cell subsets in tumor-bearing mice showed the absolute dependence of the antitumor response on CD4+ cells, whereas tumor rejection was unaffected by depletion of CD8+ cells. In addition to CD4+ cells, CR3+ cells were also needed for tumor rejection. The antitumor effect of IL-7 was confirmed by expression of the IL-7 gene in a second tumor cell line of different cellular origin. Together, our results demonstrate that a high local IL-7 concentration at the tumor site obtained by tumor cell-targeted gene transfer leads to tumor rejection involving a cellular mechanism that seems to be different from the ones observed in analogous experiments with other cytokines.
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DOI：
10.1084/jem.173.5.1047
发表时间：
1991-05-01
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Blankenstein T;Qin ZH;Uberla K;Müller W;Rosen H;Volk HD;Diamantstein T
通讯作者：
Diamantstein T
DOI：
10.1073/pnas.80.3.825
发表时间：
1983-01-01
期刊：
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA-BIOLOGICAL SCIENCES
影响因子：
--
作者：
OI, VT;MORRISON, SL;BERG, P
通讯作者：
BERG, P
影响因子：
64.5
作者：
FEARON, ER;PARDOLL, DM;FROST, P
通讯作者：
FROST, P
影响因子：
3.6
作者：
LI, WQ;DIAMANTSTEIN, T;BLANKENSTEIN, T
通讯作者：
BLANKENSTEIN, T
影响因子：
15.3
作者：
ROSEN, H;GORDON, S;NORTH, RJ
通讯作者：
NORTH, RJ