Rejection of RG-2 gliomas is mediated by microglia and T lymphocytes

Rejection of RG-2 gliomas is mediated by microglia and T lymphocytes
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RG-2 神经胶质瘤的排斥是由小胶质细胞和 T 淋巴细胞介导的

DOI:
10.1007/s11060-006-9137-x
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发表时间:
2006
影响因子:
3.9
通讯作者:
W. Streit
W. Streit
中科院分区:
医学2区
文献类型:
--
作者:
C. Mariani;J. Kouri;W. Streit

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免疫疗法在侵袭性脑肿瘤的治疗方面有很大的希望,我们特别感兴趣的是评估小胶质细胞的免疫刺激作为一种潜在的策略。为了更好地了解小胶质细胞的肿瘤战斗能力,我们比较了RG-2胶质瘤颅内植入后同系(Fisher 344)和同种异体(Wistar)大鼠品系的反应。通过临床检查、磁共振成像(MRI)和免疫组化对动物进行小胶质细胞和其他免疫细胞抗原的评价。虽然所有Fisher 344大鼠都发生了致命的RG-2胶质瘤,但Wistar品系的肿瘤生长缓慢,有时达到相当大的尺寸,但最终所有肿瘤都消退了。肿瘤消退与更多数量的T细胞和CD 8阳性细胞以及MHC I和CD 4阳性小胶质细胞的增加相关。我们的研究结果表明,外周和中枢神经系统内源性免疫细胞的联合动员是根除颅内大肿瘤所必需的。
SummaryImmunotherapy holds great promise for the treatment of invasive brain tumors, and we are interested specifically in evaluating immune stimulation of microglial cells as one potential strategy. In order to better understand the tumor fighting capabilities of microglial cells, we have compared the responses of syngeneic (Fisher 344) and allogeneic (Wistar) rat strains after intracranial implantation of RG-2 gliomas. Animals were evaluated by clinical examination, magnetic resonance imaging (MRI) and immunohistochemistry for microglial and other immune cell antigens. While lethal RG-2 gliomas developed in all of the Fisher 344 rats, tumors grew variably in the Wistar strain, sometimes reaching considerable sizes, but eventually all of them regressed. Tumor regression was associated with greater numbers of T cells and CD8 positive cells and increases in MHC I and CD4 positive microglia. Our findings suggest that the combined mobilization of peripheral and CNS endogenous immune cells is required for eradicating large intracranial tumors.
DOI: 10.4049/jimmunol.154.9.4309
发表时间: 1995-05
影响因子: 4.4
作者:
A. L. Ford;A. Goodsall;W. Hickey;J. Sedgwick
通讯作者: A. L. Ford;A. Goodsall;W. Hickey;J. Sedgwick
从免疫原性和非免疫原性大鼠脑肿瘤中分离出的肿瘤浸润淋巴细胞的表型和功能活性。
DOI: --
发表时间: 1991
期刊: Cancer research
影响因子: 11.2
作者:
Tzeng,JJ;Barth,RF;Orosz,CG;James,SM
通讯作者: James,SM
DOI: 10.1073/pnas.90.11.4942
发表时间: 1993-06-01
影响因子: 11.1
作者:
KOVACSOVICSBANKOWSKI, M;CLARK, K;ROCK, KL
通讯作者: ROCK, KL