Shichkin Valentin P, Moriev Roman M
Department of Immunology, University "Ukraine", 23 Lvivska Street, Building 2, Room 301, Kyiv 03115, Ukraine ; Department of Chemical and Biomolecular Engineering, Whiting School of Engineering, Johns Hopkins University, Baltimore, MD 21218, USA.
Department of Immunology, University "Ukraine", 23 Lvivska Street, Building 2, Room 301, Kyiv 03115, Ukraine.
ScientificWorldJournal. 2014 Feb 16;2014:165265. doi: 10.1155/2014/165265. eCollection 2014.
Previously, the mouse A20 B-cell lymphoma engineered to express hemagglutinin (HA) antigen (A20HA) was used as a systemic tumor model. In this work, we used the A20HA cells as a brain tumor. HA-specific CD4(+) T cells were transferred intravenously in a tail vein 5 days after A20HA intracranial inoculation and analyzed on days 2, 9, and 16 after the adoptive transfer by different methods. The transferred cells demonstrated state of activation as early as day 2 after the adoptive transfer and most the of viable HA-specific cells became anergic on day 16. Additionally, symptoms of systemic immunosuppression were observed in mice with massive brain tumors at a late stage of the brain tumor progression (days 20-24 after the A20HA inoculation). Despite that, a deal of HA-specific CD4(+) T cells kept the functional activity even at the late stage of A20HA tumor growth. The activated HA-specific CD4(+) T cells were found also in the brain of brain-tumor-bearing mice. These cells were still responding to reactivation with HA-peptide in vitro. Our data support an idea about sufficient role of both the tumor-specific and -nonspecific mechanisms inducing immunosuppression in cancer patients.
此前,经过基因工程改造以表达血凝素(HA)抗原的小鼠A20 B细胞淋巴瘤(A20HA)被用作全身性肿瘤模型。在本研究中,我们将A20HA细胞用作脑肿瘤模型。在颅内接种A20HA细胞5天后,通过尾静脉静脉注射HA特异性CD4(+) T细胞,并在过继转移后的第2、9和16天采用不同方法进行分析。过继转移后最早在第2天,转移的细胞就表现出激活状态,并且大多数存活的HA特异性细胞在第16天变得无反应。此外,在脑肿瘤进展后期(接种A20HA细胞后第20 - 24天),患有大量脑肿瘤的小鼠出现了全身免疫抑制症状。尽管如此,即使在A20HA肿瘤生长后期,仍有大量HA特异性CD4(+) T细胞保持功能活性。在荷脑肿瘤小鼠的大脑中也发现了活化的HA特异性CD4(+) T细胞。这些细胞在体外对HA肽的再激活仍有反应。我们的数据支持这样一种观点,即肿瘤特异性和非特异性机制在诱导癌症患者免疫抑制方面都发挥了重要作用。