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在用bcr-abl转化细胞攻击的DNA疫苗接种小鼠中,CD4 + T细胞而非CD8 + T细胞具有肿瘤保护活性。

Tumor protective activity of CD4+ but not of CD8+ T cells in DNA-vaccinated mice challenged with bcr-abl-transformed cells.

作者信息

Petráčková Martina, Lučanský Vincent, Vonka Vladimír

机构信息

Institute of Hematology and Blood Transfusion, Department of Experimental Virology, U Nemocnice 1, 12820 Prague 2, Czech Republic.

出版信息

Clin Dev Immunol. 2013;2013:923107. doi: 10.1155/2013/923107. Epub 2013 Nov 21.

DOI:10.1155/2013/923107
PMID:24348684
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3856117/
Abstract

In the recent past, it has repeatedly been reported that CD4 cells play an important role in the immunology of chronic myeloid leukaemia. It was therefore of interest to test their activity in an animal model using bcr-abl-transformed cells. BALB/c mice were four times immunized with a DNA vaccine carrying the bcr-abl fusion gene. Two weeks after the last vaccine dose, the animals were challenged with syngeneic bcr-abl-transformed 12B1 cells which form solid tumors after subcutaneous administration. At the time of challenge, animals were treated with antibodies against the CD8+ T cells or CD4+ T cells. The efficacy of the depletion was monitored and found highly effective. All nonimmunized animals developed tumors. All animals untreated with the antibodies as well as those in which CD8+ T cells had been depleted, were fully protected against the challenge. On the other hand, almost all mice treated with anti-CD4+ antibody developed tumors. These results strongly suggested that the CD4+ T cells acted as effectors in the present system.

摘要

最近,有多次报道称CD4细胞在慢性髓性白血病的免疫学中发挥重要作用。因此,利用bcr-abl转化细胞在动物模型中测试它们的活性很有意义。用携带bcr-abl融合基因的DNA疫苗对BALB/c小鼠进行四次免疫。在最后一剂疫苗接种两周后,用同基因的bcr-abl转化的12B1细胞对动物进行攻击,这些细胞在皮下给药后会形成实体瘤。在攻击时,用抗CD8 + T细胞或抗CD4 + T细胞的抗体对动物进行治疗。监测耗竭的效果,发现非常有效。所有未免疫的动物都长出了肿瘤。所有未用抗体治疗的动物以及CD8 + T细胞已被耗竭的动物都完全受到保护,免受攻击。另一方面,几乎所有用抗CD4 +抗体治疗的小鼠都长出了肿瘤。这些结果强烈表明,CD4 + T细胞在本系统中充当效应细胞。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f011/3856117/7bee73c572eb/CDI2013-923107.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f011/3856117/92e74000f944/CDI2013-923107.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f011/3856117/533d0c8c6e93/CDI2013-923107.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f011/3856117/7bee73c572eb/CDI2013-923107.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f011/3856117/92e74000f944/CDI2013-923107.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f011/3856117/533d0c8c6e93/CDI2013-923107.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f011/3856117/7bee73c572eb/CDI2013-923107.003.jpg

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